Showing posts with label hav. Show all posts
Showing posts with label hav. Show all posts

Friday, June 28, 2013

CDC-Multistate outbreak of Hepatitis A infections linked to pomegranate seeds from Turkey

CDC-Multistate outbreak of Hepatitis A infections linked to pomegranate seeds from Turkey
Posted June 28, 2013 2:00 PM ET

CDC is collaborating with public health officials in several states and the US Food and Drug Administration (FDA) to investigate a multistate outbreak of Hepatitis A illnesses. Results from the ongoing investigation are highlighted below.

Highlights

Epidemiologic Investigation:

Read the Advice to Consumers »
As of June 27, 2013, 127 people have been confirmed to have become ill from Hepatitis A after eating ‘Townsend Farms Organic Anti-oxidant Blend’ in 8 states: Arizona (17), California (64), Colorado (25), Hawaii (7), New Mexico (5), Nevada (5), Utah (2), and Wisconsin (2).
[Note: The cases reported from Wisconsin resulted from exposure to the product in California.]

71 (58%) ill people are women

Ages range from 2 – 84 years;
74 (61%) of those ill were between 40 – 64 years of age.
6 children under age 18 were also ill. None were previously vaccinated.
Illness onset dates range from 3/31/2013 – 6/15/2013
55 (45%) ill people (all over 18 years of age) have been hospitalized, and no deaths have been reported

All those who reported eating this product purchased it from Costco markets; however, the product was also sold at Harris Teeter stores. No cases have been identified that bought the product at Harris Teeter at this time.

Laboratory Investigation:

The outbreak strain of hepatitis A virus, belonging to genotype 1B, was found in clinical specimens of 56 people in seven states: AZ (6), CA (15), CO (22), HI (4), NM (4), NV (4) and WI (1; the person was exposed in California). This subtype is rarely seen in the Americas but circulates in North Africa and the Middle East.

This genotype was identified in a 2013 outbreak in Europe linked to frozen berries and another 2012 outbreak in British Columbia related to a frozen berry blend with pomegranate seeds from Egypt. However, there is no evidence at this time that these outbreaks are related to the ongoing U. S. outbreak.

Regulatory Investigation:

On June 3, 2013, Townsend Farms, Inc. of Fairview, Oregon voluntarily recalled certain lots of its frozen Organic Antioxidant Blend because it has the potential to be contaminated with hepatitis A virus.

FDA is inspecting the processing facilities of Townsend Farms of Fairview, Oregon.
By combining information gained from the FDA’s traceback and trace forward investigations and the CDC’s epidemiological investigation, FDA and CDC have determined that the most likely vehicle for the Hepatitis A virus is appears to be a common shipment of pomegranate seeds from Turkey used by Scenic Fruit Company to make the recalled Woodstock Frozen Organic Pomegranate Kernels and by Townsend Farms to make the recalled Townsend Farms and Harris Teeter Organic Anti-Oxidant Blend.

The FDA reviewed records and determined that the pomegranate seeds from this shipment were the only ingredient common to all of the recalled Townsend Farms and Harris Teeter Organic Anti-Oxidant Blend.

On June 26, 2013, Scenic Fruit Company of Gresham, Oregon recalled specific lots of Woodstock Frozen Organic Pomegranate Kernels.
Combining information gained from the FDA’s traceback and trace forward investigations and the CDC’s epidemiological investigation, it has been determined that the vehicle for the Hepatitis A virus is a common shipment of pomegranate seeds from Turkey used by Scenic Fruit Company in making the recalled Woodstock Frozen Organic Pomegranate Kernels and by Townsend Farms in making Townsend Farms Organic Anti-Oxidant Blend

FDA will be working to identify and contact other food processors who may have also received pomegranate seeds from this shipment from Turkey, so that products using these seeds may be recalled.

FDA has finalized a protocol to test berries for the Hepatitis A virus, and is testing samples related to the outbreak for the presence of the virus.

According to the label, the “Townsend Farms Organic Anti-Oxidant Blend” frozen berry and pomegranate mix associated with illness contained products originating from the U.S., Argentina, Chile, and Turkey.

At a Glance:
*The cases reported from Wisconsin resulted from exposure to the product in California

Vaccine and IG Information:
Hepatitis A Vaccine Schedule
Postexposure Prophylaxis - Use of vaccine and IG
Source for IG

More Information:
Advice to Consumers & Retailers
Hepatitis A Information
Key Resources
 

Wednesday, July 25, 2012

Patients with HCV may not benefit from HAV vaccination

Rowe IA. Hepatology. 2012;doi:10.1002/hep.25683.

July 24 2012

Routine HAV vaccination in patients with HCV may not be cost-effective or beneficial to patients, according to recent study results.

In a meta-analysis of 10 studies, researchers evaluated the mortality risk from HAV superinfection among 22,371 patients with HCV who were vaccinated against HAV. Incorporated data included the type of study, data collection methods, diagnostic criteria, study length, the number of patients involved and the number of deaths attributed to HAV.

Investigators established a pooled OR of 7.23 (95% CI, 1.24-42.12) for mortality risk from HAV superinfection, which was equated with 1.4 deaths for every one million susceptible patients with HCV annually. Heterogeneity between studies was determined (I2=56%, P=.03), and this analysis excluded three studies reporting zero deaths. A subsequent analysis that incorporated all 10 studies and used a random effects model and continuity correction resulted in an OR of 6.88 (95% CI, 1.32-36.01).

Publication bias toward increased mortality risk was observed, with studies submitted as original articles reporting a higher mortality risk (OR=38.75; 95% CI, 7.33-204.84) while those published as correspondence suggested rates similar to the population risk (OR=0.86; 95% CI, 0.15-4.90).

Assuming an incidence rate of five cases of HAV superinfection for every 100,000 patients with HCV, researchers calculated the number needed to vaccinate (NNV) patients with HCV against HAV was 23,565 to prevent one case. The NNV to prevent one death annually was calculated at 814,849, with an estimated cost of $162 million for the vaccine, or $80.1 million per death prevented. Both calculations assumed a 94.3% efficacy rate and 90% uptake for the vaccine.

“These data challenge the use of routine HAV vaccination in HCV-infected persons and its incorporation into clinical practice guidelines,” the researchers wrote. “These findings highlight several key issues in the development of both guidelines and quality measures. Firstly, the assessment of the evidence and the benefit of interventions need occur in light of relevant prevalence data. Secondly, changes in prevalence need to be considered when guidelines or quality measures are revised or reassessed. Physicians otherwise run the risk of exposing many patients to interventions that are ultimately of no benefit to them.”

http://www.healio.com/hepatology/chronic-hepatitis/news/online/%7B908A09AD-8877-473A-B4BE-91C6FC423E14%7D/Patients-with-HCV-may-not-benefit-from-HAV-vaccination

Friday, September 16, 2011

Hepatitis News Ticker;Does antiviral therapy prevent hepatocellular carcinoma?

New On The Blog;

New Hepatitis C Drugs Offer Options but With Added Complications

In This Weeks News

Telaprevir-Shorter treatment



Todays HCV News

Does antiviral therapy prevent hepatocellular carcinoma?
Kwon H, Lok AS; Antiviral Therapy 16 (6), 787-95 (2011)
Source: Antiviral Ther

Chronic infection with HBV or HCV can lead to the development of hepatocellular carcinoma (HCC). The major risk factors for HBV-related HCC are persistent presence of hepatitis B e antigen (HBeAg) and/or high serum HBV DNA levels, and cirrhosis.

The major risk factor for HCV-related HCC is cirrhosis. One randomized double blind controlled trial of lamivudine in patients with HBeAg and/or high serum HBV DNA levels showed that antiviral therapy prevented disease progression and reduced the incidence of HCC.

A beneficial effect of antiviral therapy on the risk of HCC has also been shown in cohort studies and meta-analyses, particularly among responders. Several randomized controlled trials of interferon in patients with HCV-related cirrhosis showed that treated patients had a lower incidence of HCC.

A greater effect was observed in patients who achieved sustained virological response, while the benefit in non-responders is unclear. Antiviral therapies for hepatitis B and hepatitis C can prevent but not completely eliminate HCC.

Improvement in identification of infected persons, accessibility of care and affordability of treatment is needed for antiviral therapy to have a major impact on the global incidence of HCC.

Ribavirin priming improves the virological response to antiviral treatment in transplanted patients with recurrent hepatitis C: a pilot study
Merli M, Giannelli V, Gentili F, Giusto M, Simmaco M, Lionetto L, Corradini SG, Biliotti E, Attili AF, Rossi M, Taliani G; Antiviral Therapy 16 (6), 879-85 (2011)

INTRODUCTION
Patients with hepatitis C recurrence after liver transplantation represent a clinical challenge. Antiviral treatment in transplant patients has usually poor tolerability and limited efficacy, with a mean sustained virological response (SVR) of 30%. Our pilot study was aimed at evaluating whether 8-week ribavirin pre-treatment could increase either adherence or antiviral effect of a 48-week combination therapy.

METHODS
Ribavirin pre-treatment (8 weeks) was started with 600 mg daily and increased to 10.4 mg/kg/day. After pre-treatment, 1.5 μg/kg/week pegylated interferon-α2b was added for 48 additional weeks of combination therapy. Blood count, liver function tests and plasma HCV-RNA were examined monthly. Ribavirin plasma concentrations were determined by HPLC.

RESULTS
Thirteen patients (mean age 53 ±2 years, 11 males) were treated: eight were HCV genotype 1/4; five were genotype 2/3. The median baseline HCV RNA level was 6.5 log (10) (range 5.84-7.42 log (10) ). During ribavirin pre-treatment the median HCV RNA levels decreased significantly (5.7 log (10) ; P=0.023). During combination therapy 6/13 (46%) patients exhibited a rapid virological response (RVR) and 10/13 (77%) patients a complete early virological response, two were non-responders. A decline of 0.5 log (10) HCV RNA during pre-treatment predicted RVR. SVR occurred in six patients (46%): four were genotype 2/3. Stable ribavirin dose reduction was required in only two patients (15%) in whom transient interferon reduction was also required.

CONCLUSION
This proof-of-concept study indicates that ribavirin pre-treatment increased the tolerability of the antiviral treatment, and improved its efficacy in liver transplant patients. Moreover, the degree of HCV RNA decline during pre-treatment allowed one to predict on-treatment response.

Analysis of the Complete Open Reading Frame of Genotype 2b Hepatitis C Virus in Association with the Response to Peginterferon and Ribavirin Therapy
Patients infected with genotype 2b hepatitis C virus (HCV) generally can achieve favorable responses to pegylated-interferon plus ribavirin therapy (PEG-IFN/RBV). However, a proportion of patients show poorer responses and the correlation between viral sequence variation and treatment outcome remains unclear.The pretreatment complete open reading frame (ORF) sequences of genotype 2b HCV determined by direct sequencing were investigated for correlation with the final outcome in a total of 60 patients...Full Text

Related; RSS From PLoS ONE Blog

From Expert Review of Anti-Infective Therapy
Management of Viral Infections in Solid Organ Transplant Recipients
Raymund R Razonable
Authors and Disclosures
Posted: 09/16/2011; Expert Rev Anti Infect Ther. 2011;9(6):685-700. © 2011 Expert Reviews Ltd.

Introduction Only
Click Here For Full Text
Viruses are major pathogens that cause morbidity and mortality after solid organ transplantation (SOT). Some of these infections generally follow a stereotypical temporal pattern. The first month after SOT represents the period when herpes simplex virus (HSV)-seropositive transplant recipients are at highest risk of HSV-1 and HSV-2 infection.[1] Other viruses that present during this time are often donor derived, such as the rare transmission of West Nile virus, rabies virus and lymphocytic choriomeningitis virus.[2–4] The classic 'opportunistic' viral pathogens typically occur during the second to the sixth months after SOT, when impairment in cell-mediated immunity is most intense; primary or reactivated cytomegalovirus (CMV) disease is most common during this period.[5–9] During the 'late period,' which begins more than 6 months after SOT, Varicella zoster virus (VZV) may reactivate to cause mono- or multidermatomal zoster or disseminated disease. Liver recipients with chronic viral hepatitis B and C may have an accelerated course that progresses to allograft failure.[10–14]


Late-onset CMV disease, with either classic or atypical presentation, may also occur.[15–21] Adenoviruses and community-acquired respiratory viruses such as respiratory syncytial virus (RSV), influenza virus and parainfluenza virus occur anytime after SOT, but with the risk of severe illness and outcome during the first 3 months.[22,23]

Epstein–Barr virus infection may occur anytime after SOT to cause post-transplant lymphoproliferative disorders (PTLDs).[9,24] In endemic regions, human herpesvirus 8 (HHV-8) reactivation may lead to the development of Kaposi's sarcoma (KS). In this article, the current management of virus infections after SOT are discussed, with particular focus on herpes, hepatitis, polyoma and RNA viruses causing respiratory diseases... Continue Reading..

Ask the Doctor: What is Hepatitis and HIV co-infection?
Hepatitis is a viral infection that attacks liver cells. There are three main types of hepatitis: A, B and C. Hepatitis A is a liver infection caused by a virus that does not produce long-term or chronic liver problems... Continue Reading..

T cells making brain chemicals may lead to better treatments for inflammation, autoimmune diseases
MANHASSET, NY -- Scientists have identified a surprising new role for a new type of T cell in the immune system: some of them can be activated by nerves to make a neurotransmitter (acetylcholine) that blocks inflammation. The discovery of these T cells is novel and suggests that it may be possible to treat inflammation and autoimmune diseases by targeting the nerves and the T cells. The study was published this week in Science.

"The discovery that 2 percent of T cells can make acetylcholine under the control of nerves gives a new insight into how the nervous system regulates immunity," said Kevin J. Tracey, MD, president and chief executive officer of The Feinstein Institute for Medical Research, and principal investigator of the study. "The arrival of electrical signals from nerves activates these specialized T cells to produce the acetylcholine necessary to block inflammation, and protect against damage. It is possible to transfer these cells to cross-protect mice from inflammation, and to control these T cells by electrically stimulating the nerves directly."

The present study followed years of work from Dr. Tracey's lab that identified the role of the vagus nerve, named for its wandering course from the base of the brain to the liver, spleen and other organs, in blocking inflammation. Applying electrodes to stimulate the vagus nerve blocked the release of tumor necrosis factor (TNF) and other cytokines that underlie the tissue damage in arthritis, inflammatory bowel disease and other syndromes. Stimulating this nerve pathway led to increased production of acetylcholine, a neurotransmitter that binds to the alpha 7 nicotinic acetylcholine receptor. Activating this receptor on macrophages blocked the release of immune molecules (the cytokines,) suggesting a novel strategy for developing anti-inflammatory agents.

But these results raised an important question because the nerve fibers in spleen release norepinephrine, another neurotransmitter, but not acetylcholine. The search for the cells that produce acetylcholine led these investigators to use "nude" mice, devoid of T cells. Then they examined the spleen cells that make acetylcholine and that led them to a subset of T cells. Transferring these acetylcholine producing T-cells into nude mice restored the vagus nerve circuit that blocked inflammation.

"Our results point to a population of acetylcholine-synthesizing memory T cells in spleen that is integral to the function of the inflammatory reflex, the nerve circuit that regulates inflammation and immunity," said Dr. Tracey. "It is as if these T cells occupy a nerve-like function in this important circuit."

It should be possible to target these T cells and to modulate this neural circuitry to develop therapeutic modalities for inflammatory and autoimmune diseases. In the future, it may be possible to isolate these T cells and exploit their anti-inflammatory activity. In the meantime, there is a more direct route to use this discovery for therapy. Rheumatoid arthritis patients in Europe are being studied in clinical trials where vagus nerve stimulators are implanted and turned on to stimulate this circuit and suppress inflammation.
###
About The Feinstein Institute for Medical Research Headquartered in Manhasset, NY, The Feinstein Institute for Medical Research is home to international scientific leaders in Parkinson's disease, Alzheimer's disease, psychiatric disorders, rheumatoid arthritis, lupus, sepsis, inflammatory bowel disease, diabetes, human genetics, leukemia, lymphoma, neuroimmunology, and medicinal chemistry. The Feinstein Institute, part of the North Shore-LIJ Health System, ranks in the top 6th percentile of all National Institutes of Health grants awarded to research centers. For more information: http://www.feinsteininstitute.org/

This video covers Hepatitis A after exposure

*Remember that chronic liver disease puts you at risk for serious complications if you get infected with the hepatitis A virus.

Dr. Ron Warner answers viewers questions about Hepatitis A
Ron Warner, Ph.D., is an Infectious Disease Specialist and Professor at the Texas Tech Health Sciences Center. He has provided this information to our viewers in addition to the questions he answered in our segment on NewsChannel 11 at Ten.
-Karin McCay







Media

37 students stabbed with needle in Puerto Rico
By Danica Coto, Associated Press
SAN JUAN, Puerto Rico — A 14-year-old girl went on a playground rampage with a hypodermic needle, stabbing 37 classmates, Puerto Rican officials said Thursday."She would stab one, run, stab another, run, like it was some sort of joke," Education Secretary Jesus Rivera Sanchez said about Tuesday's lunchtime attack on 12- to 14-year-olds at the Jose de Choudens middle school in the southern coastal town of Arroyo.Health Department spokeswoman Margarita Casalduc said it was unclear if the syringe contained anything and further tests were needed to determine if it was contaminated.But the victims, accompanied by their shaken parents, gathered at a convention center to be tested for HIV and hepatitis C and to be given preventive medications.Sanchez said counselors also were helping the victims and their parents.

Social workers were interviewing the alleged attacker to try to determine a motive, Justice Department spokesman Fidel Rodriguez said. He said no charges had yet been filed, but officials said she had been suspended from school.Rivera said the girl first told investigators she found the syringe, but later said she stole an unused one while visiting a relative at a hospital and had planned to pierce her ear with it. He said it was not clear why she decided to attack her classmates.A woman who answered the phone at the school said the director, Gloria Ramos, was not available for comment.

Pharmaceutical

Teva bets $7.5M on hep C program at upstart Cocrystal
As the generic drug giant pushes to capitalize on more novel therapies, Teva Pharmaceutical ($TEVA) has invested an initial $7.5 million in Bothell, WA-based developer Cocrystal Discovery to advance its work on new drugs targeting the hepatitis C virus. If it likes what it sees, Teva has the option to pump more money into the upstart, which is focused on small-molecule antiviral drugs.
Hep C has attracted lots of pharma investment due to the white-hot market opportunity for developing oral drugs that home in on viral replication enzymes. Upping its bet on the hep C game after Vertex ($VRTX) and Merck ($MRK) hit the market this year with protease inhibitors against the liver-wrecking virus, Teva has gained an option for exclusive development rights to Cocrystal's drug. The generic drugmaker also has the option to back Cocrystal's development of antiviral drugs for other diseases. The start-up now has programs in influenza and the common cold... Continue Reading...

Will the UN backtrack on accessible medicine?
The US and Europe are pushing the UN to flout the Doha Declaration, which improves poorer countries' access to drugs.
The term "compulsory license" is used to describe cases in which governments or courts set aside the exclusive rights of a patent, and allow others to use inventions, normally in return for a royalty payment to the patent owner. In such cases, the patent is no longer an absolute monopoly to use the invention, but does ensure that patent owners are paid when the inventions are used by third parties.
The use of compulsory licenses are as old as the patent system itself (a 1474 Venetian statute and an English law passed in 1623 both sanctioned compulsory licenses), and are used in a wide range of cases. While maintaining an active trade policy to prevent developing countries from using compulsory licenses for patents on medicines, at home the United States has used compulsory licenses to expand access to patented inventions to treat cancer, diagnose the Hepatitis C virus, manufacture contact lenses, and treat aortic valve heart disease.

Health Insurance

Helping the uninsured sign up for health insurance
As you may have heard, a new nonprofit group launched yesterday to help get Americans – specifically those who, beginning in 2014, will be eligible for coverage under the Affordable Care Act – signed up for insurance. Enroll America, a coalition of 42 companies and organizations, is planning a state-by-state publicity campaign and will launch an effort to help state leaders “put in place procedures to simplify enrollment.” (Its website also offers resources for people currently looking for coverage.) Over at Wonkblog, Sarah Kliff tells readers they should keep an eye on the group:
Enroll America is taking on a challenging issue on in a big way. The majority of uninsured Americans don’t think the health reform law will help them, the most recent Kaiser Family Foundation report found.As the Hill’s Sam Baker smartly pointed out, polling data seems to show Americans forgetting what the reform law does as we move further away from its passage. “Our biggest hurdle is most people don’t even know this is coming,” says Rachel Klein, director of Enroll America. How much a multi-million campaign can change that will be a key factor to watch in the health law’s success... Continue Reading...

FYI

Tempest In A Lunch Box: Arsenic Traces In Apple Juice
A lot of parents might be worried about what's in their kids' sippy cups if they caught a recent report by TV talk show host Dr. Mehmet Oz about high levels of arsenic in popular brands of apple juice.
But the Food and Drug Administration and medical experts are attacking Oz's report, saying it's inaccurate and needlessly panics parents.

Monday, August 15, 2011

What Factors Determine the Severity of Hepatitis A-related Acute Liver Failure?

From Journal of Viral Hepatitis
What Factors Determine the Severity of Hepatitis A-related Acute Liver Failure?
V. Ajmera; G. Xia; G. Vaughan; J. C. Forbi; L. M. Ganova-Raeva; Y. Khudyakov; C. K. Opio1, R. Taylor; R. Restrepo; S. Munoz; R. J. Fontana; W. M. Lee
Authors and Disclosures
Posted: 08/15/2011; J Viral Hepat. 2011;18(7):e167-e174. © 2011 Blackwell Publishing

Abstract and Introduction
Abstract
The reason(s) that hepatitis A virus (HAV) infection may progress infrequently to acute liver failure are poorly understood. We examined host and viral factors in 29 consecutive adult patients with HAV-associated acute liver failure enrolled at 10 sites participating in the US ALF Study Group. Eighteen of twenty-four acute liver failure sera were PCR positive while six had no detectable virus. HAV genotype was determined using phylogenetic analysis and the full-length genome sequences of the HAV from a cute liver failure sera were compared to those from self-limited acute HAV cases selected from the CDC database. We found that rates of nucleotide substitution did not vary significantly between the liver failure and non-liver failure cases and there was no significant variation in amino acid sequences between the two groups. Four of 18 HAV isolates were sub-genotype IB, acquired from the same study site over a 3.5-year period. Sub-genotype IB was found more frequently among acute liver failure cases compared to the non-liver failure cases (chi-square test, P < 0.01). At another centre, a mother and her son presented with HAV and liver failure within 1 month of each other. Predictors of spontaneous survival included detectable serum HAV RNA, while age, gender, HAV genotype and nucleotide substitutions were not associated with outcome. The more frequent appearance of rapid viral clearance and its association with poor outcomes in acute liver failure as well as the finding of familial cases imply a possible host genetic predisposition that contributes to a fulminant course. Recurrent cases of the rare sub-genotype IB over several years at a single centre imply a community reservoir of infection and possible increased pathogenicity of certain infrequent viral genotypes.

Introduction
Hepatitis A virus (HAV), a single stranded RNA virus, is endemic throughout most of the world and is also highly genetically conserved.[1,2] In the United States, rates of infection have dropped significantly with increased use of the hepatitis A vaccine, however the estimated incidence is still above 30 000 new infections per year.[3] The infection usually follows an innocuous course, remaining sub-clinical in most children, while appearing as acute self-limited hepatitis in adults. Less than 1% of acute hepatitis A cases result in acute liver failure.[4,5] HAV infection currently accounts for only 3% of adult acute liver failure (ALF) cases in the United States.[4,6] Although hepatitis A-related ALF patients experience a relatively high spontaneous survival rate (69%), the remaining patients either die or require emergency liver transplantation.[7]

The relationship between self-limited hepatitis A cases and those HAV infections resulting in ALF (HAV ALF) is poorly understood. Host factors including age and underlying liver disease are thought to increase the likelihood of a fulminant course.[8,9] Viral factors including low viral load and a higher rate of substitution in the 5' untranslated region (UTR) of the viral RNA have also been correlated with increased frequency of HAV-related ALF.[10,11] Another potential viral factor is genotype. Epidemiologic studies in the United States have demonstrated that sub-genotype IA is most common, comprising 98% of infections, while sub-genotype IB is found in only 2%; most IB infections have been associated with international travel.[12] To date, no correlation between ALF and HAV genotype has been evident but this has not been systematically examined. Previous studies have focused on the 5' UTR and VP1-P2B regions, while only small case series have evaluated the entire HAV genome of HAV ALF cases.[13] This study aimed to further explore both host and viral factors, including genotype and nucleotide sequence variation in the entire HAV genome among consecutive adult cases of HAV ALF from the multicentre adult US acute liver failure registry. To identify factors contributing to variation in outcomes, full genome sequences of 18 HAV ALF cases were compared to geographically matched controls: patients with self-limited acute HAV identified in the CDC database.

Patients and Methods
The adult US Acute Liver Failure Study Group (ALFSG) is a cooperative effort of 23 tertiary liver centres to study the aetiology and outcomes of ALF.[14] Twenty-nine patients from the ALFSG registry were diagnosed with HAV ALF between January 1998 and May 2004 and all of these patients were included in this study. ALF was defined as the onset of encephalopathy and coagulopathy within 26 weeks of first symptoms of hepatic illness with no prior history of liver disease.[15] Encephalopathy was defined as any degree of altered mentation while coagulopathy was defined by an international normalized ratio (INR) ≥1.5. ALF was attributed to acute HAV infection when a positive IgM anti-HAV antibody test was obtained in conjunction with consistent clinical findings by the site investigator and the data-coordinating centre. All patients tested negative for other markers of acute viral infection including HBsAg, anti-HBc IgM, anti-HCV with the exception of two patients. One had typical acute HAV infection but was hepatitis C virus (HCV) antibody positive without detectable HCV RNA on repeated testing, unlikely to represent acute hepatitis C. One patient had evidence of both chronic hepatitis B and C with detectable HBsAg, anti-HCV, HBV DNA and HCV RNA detected but was shown to be anti-HAV IgM positive and recovered fully from ALF.

Informed consent, approved by the Institutional Review Board of each of the respective centres, was obtained from the next of kin due to the patients' altered mental status and all cases were coded to maintain anonymity. Detailed data including the patients' demographics, history, laboratory results, and outcome were obtained. Sera were collected daily for up to 7 days, stored at −80 °C and shipped to the central repository for continued storage prior to testing.
A series of randomly selected sera from US and Mexican patients with acute hepatitis A infection in the CDC database was used as controls for the HAV whole-genome analysis. These control sera included 20 sub-genotype IA and 8 sub-genotype IB specimens obtained over a similar time frame from a comparable US geographic distribution as the HAV ALF cases.

HAV RNA Amplification and Sequencing
Serum samples (collected on day 1 or no later than day 4) were available from 24 of 29 patients. These samples were used for HAV whole-genome amplification. HAV surveillance databases at the Division of Viral Hepatitis, Centers for Disease Control and Prevention, Atlanta, GA, USA were accessed to form a demographically comparable control group of acute hepatitis cases for comparison of the entire viral RNA genome. RNA was extracted using the Total Nucleic Acid Isolation kit in conjunction with a MagNAPure LC system (Roche Applied Science, Indianapolis, IN, USA). Extracted RNA was used as a template in a one step RT-PCR reaction (QIAGEN, Valencia, CA, USA) to amplify 14 different overlapping fragments encompassing the entire length of the HAV genome. Nested PCR was carried out for each amplicon to generate fragments suitable for sequencing. Sequencing of both DNA strands was carried out with the corresponding internal primers using BigDye v3.1 chemistry (Applied Biosystems, Foster City, CA, USA). The resulting products from the sequencing reaction were cleaned using the Millipore Montage SEQ96 Cleanup Kit (Millipore, Billerica, MA, USA) and later run on 3130xl Genetic Analyzer (Applied Biosystems). All reactions were performed on a Biomek 3000 Laboratory Automation Workstation (Beckman Coulter, Fullerton, CA, USA). Sequences were assembled and preliminarily analysed using SeqMan and MegAlign programs from the Lasergene DNA & Protein analysis package v8.0.2 (DNASTAR Inc., Madison, WI, USA) The Accelrys GCG Package v11.0 (Accelrys Inc. San Diego, CA, USA) was used for phylogenetic analysis. Shannon entropy was expressed as mean + standard deviation (SD). Differences in Shannon entropy and viral genetic identity were tested by ANOVA. sas for Windows version 9.2 (SAS Institute Inc., Cary, NC, USA) was used for statistics analysis.

Measurement of Acetaminophen Protein Adducts
Adducts in sera were measured using a high-performance liquid chromatography method with electrochemical detection as previously described.[16,17]

Results
Epidemiological Data
The 29 patients were obtained from 10 of the 23 ALFSG sites; demographic and laboratory data are shown in Table 1. Four patients with sub-genotype IB were from the same site (site 23, University of Michigan) and presented over the course of 3.5 years. That same site demonstrated one sub-genotype IA case during the study period as well. Site 35, Albert Einstein Medical College, recorded two related HAV ALF patients admitted within 1 month of each other, a mother and son. The mother's infection preceded the son's. Although they did not live together they had shared meals during the mother's period of infection. There were no other known interactions between patients or common risk factors other than geographic location and none of the patients had migrated from an endemic area outside of the United States.

Patient Outcomes
Sixteen of twenty-nine (55%) patients recovered spontaneously (e.g. without transplantation). Nine of twenty-nine (31%) received a liver transplant and eight survived at least 3 weeks post transplant. Four of twenty-nine patients (14%) died from renal failure, brain oedema, respiratory failure or cardiac arrest.

HAV Genetic Analyses
Eighteen of twenty-four (75%) samples were RT-PCR positive (Table 1). To confirm the PCR negative results, we repeated testing on later (day 3) samples. Five of the six remained negative. The entire genome of 15 of the 18 initially PCR positive cases was sequenced. Within the three cases that could not be completely sequenced; the VP1-P2B (nt 2912–3277) region and 5' UTR were sequenced successfully. Based on phylogenetic analysis of the VP1-P2B region 14 cases were classified as sub-genotype IA and 4 cases as sub-genotype IB. The complete HAV-genome sequences of the 15 ALF cases were compared with a control group of sequences of sub-genotype IA (n = 20) and sub-genotype IB (n = 8) retrieved from the CDC surveillance databases of acute hepatitis A cases (Fig. 1). The nucleotide and amino acid sequences were compared between ALF cases and controls within the same sub-genotype. There were no apparent sequence differences or specific nucleotide/amino acid substitutions between ALF cases and controls. Also, no significant differences by ANOVA were observed in the Shannon entropy and genetic similarity between the ALF case and control sequences among sub-genotype IA. The mean nucleotide identity among ALF cases and control sequences were 96.8 per 100 nucleotides (SD = 1.78) and 96.6% (SD = 1.81) among the sub-genotype IA (ANOVA, P = 0.447; Table 2).

However, similar analyses of the HAV sub-genotype IB sequences showed a higher nucleotide and amino acid identity among HAV variants from ALF cases than controls (ANOVA, P < 0.01; Table 2). Rates of spontaneous survival were not significantly different between the two sub-genotypes (chi-square test, Table 3).

PCR Negative Cases
The six PCR negative samples had viral loads below the lower limit of detection of the assay of 0.1 plaque forming units/100 μL.[18] PCR negative patients experienced worse outcomes than those who were PCR positive (Table 3); transplant free survival amongst PCR positive cases was 77.8% while PCR negative cases experienced a transplant free survival of 16.7% (chi-square test, P < 0.01). Being PCR positive was associated with a decreased risk of death or transplant with an odds ratio of 0.057 (95% confidence interval 0.005–0.641, P = 0.02). Of interest, the PCR negative cases as a group had lower mean peak ALT levels: 1414 IU/L compared to 3113 IU/L for the PCR positive ALF patients. Prothrombin time/international normalized ratio (INR) values were slightly more prolonged: 3.9 in the PCR negative patients vs 2.9 for PCR positive cases.

HAV Genotype IB
Four out of eighteen (22%) of the PCR positive ALF patients were infected with sub-genotype IB, which is rare in the United States. Though not identical, the sequences were remarkably similar although the cases occurred over a three and a half year period. None of the patients were born abroad nor had they visited countries where genotype IB is more common. During the same observation period (1998–2004), only 19 (2.2%) sub-genotype IB cases were detected in the United States among 834 hepatitis A cases identified through different surveillance projects and this was also highly significant (P < 0.01) by chi-square test.

Patient Co-factors
Case report data revealed that 12 of 29 patients (41.4%) reported having taken more than 1g of acetaminophen/day for at least 3 days preceding hospital admission (Table 1), therapeutic dosing that might indicate possible toxicity in the setting of viral hepatitis. Four patients reported regular alcohol consumption (>2 drinks per night), one of whom also took acetaminophen. There was no correlation between a history of acetaminophen use and poorer outcomes. Acetaminophen adducts were measured in all 24 for whom sera were available; 20 were undetectable and four demonstrated levels below 1.0 nmol a-cys adducts/mL (range 0.18–0.34). None were considered compatible with liver toxicity due to acetaminophen.[16] A more detailed clinical description of these cases has been published recently. As in our prior report of the same 29 cases, subject age, gender, and MELD score were not predictive of patient outcomes.[19]

Discussion
Since prior studies had suggested a possible difference in viral substitutions between HAV ALF patients and other patients with acute HAV, we were interested in further exploring whether unique viral genome patterns might predispose hepatitis A patients to liver failure. We did not find a clear difference in genomic sequences between patients with HAV ALF and those with self-limited hepatitis A.

The rates of single nucleotide substitutions in the complete HAV genome including both the 5' UTR and the VP1-P2B regions showed no significant variation between those with HAV ALF and patients with uncomplicated acute hepatitis A infection. This finding suggests that variation in severity of hepatitis A infection is not dependent upon rates of substitution in the internal ribosomal entry site of the 5' UTR or elsewhere in the genome. Furthermore, the differences in rates of substitution in the transcribed amino acid residues were also not significant in the two groups (Table 2).

Only a small fraction (8%) of acute HAV sera from a previous large CDC cohort study was shown to be PCR negative during the acute illness.[12] Among our HAV ALF study patients, 25% (6/24) were PCR negative and this status correlated with significantly worse outcomes defined by a lower rate of spontaneous survival. The inability to obtain PCR products in our study corresponds with an undetectable or very low viral load. Low or undetectable viral load at presentation has been previously cited as a significant factor differentiating fulminant from non-fulminant cases for both hepatitis A[11] and hepatitis B.[20] In vitro studies suggest that the immunologic response is primarily responsible for the liver disease in HAV infections.[21] In our study, undetectable viral load not only correlated with more severe disease, but also indicated a worse outcome amongst the ALF cases. However, the small number of patients with undetectable HAV RNA may limit the generalizability of this finding. Quantitative PCR was not available for this study.

With regard to use of acetaminophen, 12 of 29 patients gave a history of acetaminophen ingestion of at least 1 g/day for a minimum of 3 days (Table 1). We could not relate a history of acetaminophen ingestion to poorer outcomes or to more severe disease in this small case series, nor could we identify other demographic or clinical factors such as age or gender to be associated with poor outcome (Table 1).

Additional data were obtained on two clusters of HAV ALF cases with highly conserved viral RNA genomes. The first revealed a mother and son, both of whom presented with HAV ALF within 1 month of each other to the same clinical centre and without pre-existing liver disease. Although they did not live together, they shared meals together during the time of the first patient's infection and the close genetic similarity of their viruses confirms that infection appears to have been transmitted from mother to son. HAV ALF cases transmitted between family members have been reported in the literature, specifically the occurrence of HAV ALF among siblings.[22,23] Often the virus was transmitted to the family via a community outbreak of routine HAV infections, suggesting that host factors contributed to these more severe outcomes. Furthermore, all reported inter-familial occurrences of HAV ALF have been among patients with no pre-existing liver condition. In both previously reported studies of siblings, the infections occurred in young patients whose age ranged from 16 to 24 years. Genetic predisposition to a fulminant course could be a factor considering the inter-familial HAV ALF outbreak we observed in our study, emphasizing the possible importance of the immunological response to outcome.
A second cluster of HAV ALF cases came from a single centre. Four of five cases from this site were sub-genotype IB, which occurs very infrequently in the United States. This finding coincides with epidemiological data from typical acute hepatitis A cases that suggest that community reservoirs of infection may be present for long periods of time under certain circumstances.[12] The near identity of all four IB sequences, coupled with the rarity of genotype IB, suggest ongoing transmission of this one strain within the community and that it may be somewhat more virulent than other subtypes but this remains highly speculative.
Our study was limited in that we had serum samples on only 24 of the 29 patients with HAV ALF in the study. In addition, we could not perform phylogenetic analysis on five of the six patients because they were PCR negative repeatedly during the study period. Finally, the case controls used in this analysis of whole genome sequencing were not obtained from the same local hospital as the ALF index case due to the limited number of annual HAV cases that the CDC has access to. Nonetheless, matching based upon medical centre location and year of infection was undertaken. The small number of cases in this study of acute liver failure provides further evidence of the declining incidence of HAV infection in the United States.[19]

In conclusion, viral factors including substitution rate in the entire genome do not seem to differ between HAV ALF patients and those with uncomplicated hepatitis A infection in North America. While this study is limited in the number of cases presented, the rapidly declining rate of HAV and HAV associated ALF make it unlikely that larger studies will be possible in the future at least in the United States. However, further analysis of genotype I should be performed, particularly in locations where HAV is still endemic. An undetectable viral load at the onset of liver failure correlated in our study with worse outcomes. HAV RNA testing by PCR, if it were readily obtainable, might help determine prognosis but should not be used to preclude referral and listing for transplantation. The association of undetectable viral load with poor outcome suggests a genetic predisposition to a 'excessive' host immune response contributes to the more severe disease observed. This is further supported by the occurrence of familial ALF case clustering. Whole genome sequence analyses of patients with ALF of diverse aetiologies compared to ethnically matched controls may prove useful in identifying the genetic basis for differences in outcomes with hepatotrophic viruses.[24]

Abstract and Introduction
Patients and Methods
Results
Discussion
References

Friday, February 4, 2011

First Duplex Test for Parvovirus B19 and Hepatitis A Virus

First Duplex Test for Parvovirus B19 and Hepatitis A Virus Now Available in the US

PLEASANTON, Calif., Feb. 4, 2011 /PRNewswire/ -- Roche (SIX: RO, ROG; Pink Sheets: RHHBY) announced today that the cobas® TaqScreen DPX Test for use on the cobas s 201 system is now available in the US. It is the first commercial test to quantify parvovirus B19 and detect hepatitis A virus (HAV) simultaneously in one assay in human plasma.

Human plasma is used to create treatments for life-threatening and chronic diseases and disorders such as hemophilia and primary immunodeficiency diseases. Plasma is also used to treat patients who have suffered severe burns or trauma and has many other therapeutic uses.
"The launch of this test is an important part of our strategy," said Paul Brown, Head of Roche Molecular Diagnostics, "not only is it an important test for the continued safety of plasma products, but it also indicates our continued commitment to this vital area."
The test is a state-of-the-art, in vitro nucleic acid amplification technology (NAT) test which offers complete coverage of all human genotypes of parvovirus B19 (genotypes 1, 2 and 3 DNA) and HAV (genotypes I, II and III RNA) in human plasma.

The cobas® TaqScreen DPX Test uses multi-dye, real-time polymerase chain reaction (PCR) technology which allows for the simultaneous detection and identification of individual viral targets without the use of additional discriminatory tests. A further innovative aspect of this test is that facilitates quantification of the parvovirus B19 while detecting extremely low levels of HAV.

Both parvovirus B19 and HAV are difficult to inactivate by traditional methods used by the plasma industry and there have been reports on the transmission of HAV and parvovirus B19 through blood and plasma products. Both parvovirus B19 and HAV in human plasma can be detected by NAT during the manufacturing process of plasma products, so improving the safety of these products.

About Roche Blood and Plasma Screening
Roche is a leader in the global NAT blood and plasma screening market, which is estimated at almost 900 million CHF. Nucleic acid-based tests enable earlier detection of active viral infections than conventional antibody or antigen assays. Roche's real-time PCR-based nucleic acid assays have been used since 1998 to screen blood and plasma products. Currently, more than 225 blood banks worldwide use Roche's automated cobas s 201 system.
About Roche

Headquartered in Basel, Switzerland, Roche is a leader in research-focused healthcare with combined strengths in pharmaceuticals and diagnostics. Roche is the world's largest biotech company with truly differentiated medicines in oncology, virology, inflammation, metabolism and CNS. Roche is also the world leader in in-vitro diagnostics, tissue-based cancer diagnostics and a pioneer in diabetes management.

Roche's personalized healthcare strategy aims at providing medicines and diagnostic tools that enable tangible improvements in the health, quality of life and survival of patients. In 2010, Roche had over 80,000 employees worldwide and invested over 9 billion Swiss francs in R&D. The Group posted sales of 47.5 billion Swiss francs. Genentech, United States, is a wholly owned member of the Roche Group. Roche has a majority stake in Chugai Pharmaceutical, Japan. For more information: www.roche.com.

All trademarks used or mentioned in this release are legally protected by law.
(1) The cobas® TaqScreen DPX Test is not an FDA-licensed product.
For further information please contact:
Marianne van Zeeland
Roche Molecular Diagnostics Communications
+1 925-549-1232 (Mobile)
marianne.van_zeeland@roche.com
SOURCE Roche Molecular Systems
RELATED LINKShttp://www.roche.com

Thursday, January 27, 2011

Seroprevalence Of Anti-HAV Among Patients With Chronic Viral Liver Disease



Seroprevalence Of Anti-HAV Among Patients With Chronic Viral Liver Disease

Hepatitis A virus (HAV) is an epidemiologically important virus with a worldwide distribution and causes acute hepatitis in humans. Acute HAV superinfection causes severe liver disease, acute liver failure and even higher mortality rates in patients with underlying chronic liver disease (CLD).

Numerous studies have identified CLD as a risk factor for fulminant hepatitis and death from acute HAV infection. A research article published in the World Journal of Gastroenterology addresses this question.

In this study, the authors investigated the current seroprevalence of HAV antibodies (anti-HAV) in patients with chronic viral liver disease in South Korea.

They also tried to determine the age-specific seroprevalence in these patients to assess whether vaccination against HAV is necessary in all patients who have underlying viral liver diseases, and to determine the factors that affect IgG anti-HAV seropositivity.

This study showed that the overall prevalence of IgG anti-HAV in Korean patients with chronic viral liver disease was 86.61%, and most patients who are above 40 years of age have already been exposed to HAV.

Therefore, vaccination against HAV should be considered, particularly for young anti-HAV-negative patients with chronic liver disease. Reference: Cho HC, Paik SW, Kim YJ, Choi MS, Lee JH, Koh KC, Yoo BC, Son HJ, Kim SW. Seroprevalence of anti-HAV among patients with chronic viral liver disease.

World J Gastroenterol 2011; 17(2): 236-241

Sunday, December 5, 2010

Hepatitis A




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Jerry's Deli worker infected by hepatitis A
Posted on December 2, 2010 by Drew Falkenstein


Customers of Jerry's Famous Deli, an LA institution near the UCLA campus, may be at risk for developing hepatitis A infection if they ate there during the month of November. An employee of the Westwood deli, located at 10925 Weyburn Ave., was diagnosed with acute hepatitis A, a virus that is spread by close physical contact and through fecal contamination of food or drink. The Los Angeles Public Health Department has yet to receive any further reports of hepatitis A related to the deli.



The Department issued a press release today:
Patrons who ate sandwiches at the restaurant or who ate catered sandwiches from this location on November 18, 21, 23, or 24, 2010, should receive an immune globulin (IG) shot or a hepatitis A vaccination no later than 14 days after their exposure to prevent or reduce illness.
Public Health will make the IG shot and hepatitis A vaccine available through certain public health clinics


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Immune globulin (IG) for hepatitis A


This drug is given by injection into a muscle (intramuscular injection).


Source


How It Works
Immune globulin (IG) contains antibodies that destroy the hepatitis A virus (HAV), preventing infection.


Why It Is Used
IG should be given to unvaccinated people at risk of infection with HAV, including:
Household and sexual contacts of people diagnosed with hepatitis A.
Travelers visiting foreign countries where hepatitis A is a known problem or where sanitary conditions are questionable. Revaccination with IG is needed every 3 to 5 months. If a person frequently travels to or plans to stay for longer than 3 months in a country where hepatitis A is a problem, it is recommended that he or she receive the hepatitis A vaccine. For more information, see the Prevention section of the topic Hepatitis A.



All staff and residents of child care centers, hospitals, residences for the developmentally disabled, prisons, or food service settings where an outbreak of hepatitis A occurs.
People who need protection against HAV infection but are allergic to the vaccine.
Children younger than age 1 who need to be protected against HAV infection.


How Well It Works
If given within 2 weeks of exposure to the virus, immune globulin (IG) is more than 85% effective in preventing hepatitis A virus (HAV) infection.1
Immune globulin has been effective in controlling some outbreaks of HAV.


Side Effects


Common side effects include:
Soreness and swelling around the injection site.
Low-grade fever.
In rare cases, a life-threatening allergic reaction may occur. This is more likely if IG is accidentally injected into an artery or vein.
See Drug Reference for a full list of side effects. (Drug Reference is not available in all systems.)


What To Think About
Immune globulin (IG) is a safe, inexpensive, and effective means of preventing the spread of hepatitis A virus (HAV) infection.
The sooner you get a shot of IG after being exposed to HAV, the greater the likelihood that infection will be prevented.


IG is safe for women who are pregnant or breast-feeding.
IG protection is only temporary, lasting about 3 months. If you are planning to stay longer than 3 months in an area where hepatitis A is a problem, you should receive a higher initial dose of IG, or you should get the hepatitis A vaccine (unless you are allergic to the vaccine). You should receive the same higher dose of IG every 3 to 5 months while you are still at risk.
IG is prepared from blood products obtained from paid donors. In the United States, no cases of transmission of the human immunodeficiency virus (HIV) or hepatitis B virus (HBV) through IG have been reported. The safety of IG prepared in countries other than the U.S. cannot be guaranteed.



Complete the new medication information form (PDF)


(What is a PDF document?) to help you understand this medication.




From the Immunization Action CoalitionVaccine Informationfor the public and health professionals


, When did the first hepatitis A vaccine become available?
There are currently two hepatitis A vaccine products approved by the FDA in the United States. The first hepatitis A vaccine became available in 1995 (HAVRIX, GlaxoSmithKline), followed by the second hepatitis A vaccine in 1996 (VAQTA, Merck). They are equally safe and effective.

What kind of vaccine is hepatitis A vaccine?
Hepatitis A vaccine is an inactivated virus vaccine. No part of the vaccine is “live.”

How is hepatitis A vaccine given?
The vaccine is given by an injection into the muscle of the upper arm for adults and older children and in the thigh muscle of toddlers.

Who should get this vaccine?
Many people are recommended to receive hepatitis A vaccine, including people at increased risk for exposure to HAV infection and people who are more likely to get seriously ill if infected with HAV. According to CDC recommendations, people who should be vaccinated include:

All children at age 1 year (12-23 months)
People age 12 months or older who are traveling to or working in an area of the world except the United States, Canada, Western Europe, Japan, New Zealand, and Australia
Men who have sex with men
Users of illicit drugs, injectable or noninjectable
People who anticipate having close personal contact with an international adoptee from a country of high or intermediate endemicity during the first 60 days following the adoptee’s arrival in the United States
People who have blood clotting disorders
People who work with HAV-infected primates or with HAV in a research laboratory setting (no other groups have been shown to be at increased risk for HAV infection because of occupational exposure)
People with chronic liver disease
Any person who wishes to be immune to HAV infection
Hepatitis A vaccine is not routinely recommended for healthcare workers, sewage workers, or daycare providers. Children who are not vaccinated by age two years should be vaccinated as soon as feasible.

How many doses of hepatitis A vaccine are recommended for full protection?
Two doses are recommended. The second dose is given no sooner than six months after the first dose.

I’m not in a group for which hepatitis A vaccine is recommended. Can I still get vaccinated to protect myself against HAV infection?
Yes. Hepatitis A vaccine is safe and effective and is licensed for use in any person age 12 months and older. Any person who wishes to be immune to hepatitis A is recommended to receive the vaccine.

How long does hepatitis A vaccine protect you?
Estimates for long-term protection for fully vaccinated people (i.e., full two-dose series) suggest that protection from HAV infection could last for at least 25 years in adults and at least 14-20 years in children. Experts continue to study the long-term effectiveness of this vaccine to determine whether a booster dose will be needed.

What organizations recommend hepatitis A vaccine?
The Centers for Disease Control and Prevention, the American Academy of Pediatrics, the American Academy of Family Physicians, the American College of Obstetricians and Gynecologists, and the American College of Physicians recommend the vaccine.

Is hepatitis A vaccine safe?
Yes, hepatitis A vaccine is very safe. No serious adverse events have been attributed definitively to hepatitis A vaccine. Since the licensure of the first hepatitis A vaccine in 1995, millions of doses of hepatitis A vaccine have been distributed and administered worldwide as well as in the United States.

What side effects have been reported with this vaccine?
The most common side effect is a sore arm, which happens to one out of two adults and one out of five children. Less common side effects include headache, loss of appetite, low-grade fever, or tiredness. When these problems happen, they usually start 3–5 days after vaccination and usually last for one or two days. A very rare but serious side effect is a generalized allergic reaction. If this happens, it typically occurs within a few minutes to a few hours following the injection.

How effective is hepatitis A vaccine?
Hepatitis A vaccine is very effective. It appears that all adults, adolescents, and children become immune to HAV infection after getting two doses. After one dose, at least 94 out of 100 people become immune for the short term.

Who should not receive hepatitis A vaccine?
People who have had a serious allergic reaction to hepatitis A vaccine in the past, or who are known to be allergic to any part of the hepatitis A vaccine, should not receive it. People with moderate or severe acute illness should wait to receive hepatitis A vaccine until their condition has improved.

Can I receive hepatitis A vaccine when I am pregnant?
The answer to this question is not well studied, but because hepatitis A vaccine is produced from inactivated HAV, the theoretical risk to the developing fetus is expected to be low. The risk associated with vaccination, however, should be weighed against the risk for hepatitis A in women who may be at high risk for exposure to HAV.

Can the vaccine cause HAV infection?
No.

Is there a vaccine that protects against both HAV and HBV infections?
Yes. Twinrix, the hepatitis A and hepatitis B combination vaccine manufactured by GlaxoSmithKline, was licensed for use in the United States in 2001 for people 18 years of age and older. Three doses of Twinrix are necessary for full protection against hepatitis A and hepatitis B virus infections.

In April 2007, approval was received for an alternate 4-dose schedule for Twinrix. Using this schedule, 3 doses of Twinrix can be administered at 0, 7, and 21-30 days, followed by the 4th dose at 12 months. This schedule might benefit people needing rapid protection from both hepatitis A and hepatitis B virus infections. This includes people traveling to areas with high rates of hepatitis A and hepatitis B and emergency responders, especially those being deployed to disaster areas overseas. Again, this is available only for people 18 years of age and older.

What is immune globulin (IG)?
IG is a preparation of antibodies that can be given before exposure to HAV for short-term protection against HAV infection and to people who have already been exposed to HAV. IG must be given within 2 weeks after exposure to HAV for maximum protection.

Are there new recommendations for the use of IG and/or hepatitis A vaccine prior to travel?
Yes. All susceptible people traveling to or working in countries except the United States, Canada, Western Europe, Japan, New Zealand and Australia should receive hepatitis A vaccine or IG before departure. (If traveling to the Caribbean, people should consider getting hepatitis A vaccine or IG if travel is to areas of questionable sanitation.)

For unvaccinated people ages 1 through 40 years, the first dose of hepatitis A vaccine should be administered as soon as travel is considered, actually anytime prior to travel. The second dose should be given at least 6 months after the first dose.

For the best protection, individuals who are over age 40, immunocompromised people (e.g., people with AIDS), and people with chronic liver disease or other chronic medical conditions planning to travel in 2 weeks or less should receive the initial dose of hepatitis A vaccine and IG at the same time. The second dose of the 2-dose hepatitis A vaccine series should be given no sooner than six months after the first dose. This second dose is needed to ensure long lasting protection.

Travelers who choose not to get the hepatitis A vaccine, who are less than 12 months old, or who are allergic to the vaccine should be given IG only. The dosage of IG depends on how long you plan to be traveling and how much you weigh.

What should be done for travelers who are younger than age 12 months to protect them from HAV infection?
Recommendations have not changed for this age group as noted in the previous question. IG is recommended for travelers younger than age 12 months because hepatitis A vaccine is not licensed for use in this age group.

Can hepatitis A vaccine be given after exposure to HAV?
Yes. The recommendations for the use of hepatitis A vaccine after exposure to HAV have changed. People who recently have been exposed to HAV and who previously have not had hepatitis A vaccine should be given a single dose of hepatitis A vaccine or IG as soon as possible. Hepatitis A vaccine is preferred for healthy people age 12 months through 40 years of age. For people over 40 years of age, IG is preferred, but hepatitis A vaccine can be used if IG is unavailable. IG should be given to children younger than 12 months of age, immunocompromised people, people who have diagnosed chronic liver disease, and people for whom vaccine is contraindicated.
Questions and answers about hepatitis A disease