At first glance, the HCV lifecycle is fairly simple. The virus enters the cell. One large protein is produced and cut into several smaller viral enzymes and proteins that build the virus. The RNA genome is copied, and the new RNAs and structural proteins are used to make new virus particles that are released into the blood stream for to infect more cells. These processes were thought to occur at specialized membranes inside the cell. However, recently it has been shown that fat droplets are critically involved
The hepatitis C virus (HCV)is triggered off in its infectious activity by an enzyme connected to the fat that is stored in the liver, conclude scientists.
This discovery may offer a new strategy for treating the infection.
The study by the researchers at the Gladstone Institute of Virology and Immunology (GIVI) shows that the enzyme DGAT1 is a key factor in HCV infection.
With several potential DGAT1 inhibitors already in the drug-development pipeline, a treatment for HCV may be possible in the near future.
"Our results reveal a potential 'Achilles heel' for HCV infection," Nature quoted Melanie Ott, senio r author on the study, as saying.
"Several DGAT1 inhibitors are already in early clinical trials to treat obesity-associated diseases. They might also work against HCV," said Ott.
It has been recently shown that fat droplets are critically involved in the HCV lifecycle and DGAT1 helps in their formation.
The Gladstone team discovered that HCV infection and viral particle production are severely impaired in liver cells that lack DGAT1 activity.
"We found that HCV specifically relies on one DGAT enzymes, DGAT1. Whe we inhibit DGAT1 with a drug, the liver still produces fat droplets through another DGAT enzyme but these droplets cannot be used by HCV," said lead author Eva Herker.hey found that DGAT1 interacts with one viral protein, the viral nucleocapsid core protein, required for viral particle assembly.
The core protein normally associates with the surface of fat droplets but cannot do so when DGAT1 is inhibited or missing in infected cells.
The study was published in the journal Nature Medicine.
Source-ANI
Read more: Hepatitis C Virus Infection Contributed by Liver's Fat Enzyme http://www.medindia.net/news/Hepatitis-C-Virus-Infection-Contributed-by-Livers-Fat-Enzyme-75290-1.htm#ixzz12CpPRtCh
This discovery may offer a new strategy for treating the infection.
The study by the researchers at the Gladstone Institute of Virology and Immunology (GIVI) shows that the enzyme DGAT1 is a key factor in HCV infection.
With several potential DGAT1 inhibitors already in the drug-development pipeline, a treatment for HCV may be possible in the near future.
"Our results reveal a potential 'Achilles heel' for HCV infection," Nature quoted Melanie Ott, senio r author on the study, as saying.
"Several DGAT1 inhibitors are already in early clinical trials to treat obesity-associated diseases. They might also work against HCV," said Ott.
It has been recently shown that fat droplets are critically involved in the HCV lifecycle and DGAT1 helps in their formation.
The Gladstone team discovered that HCV infection and viral particle production are severely impaired in liver cells that lack DGAT1 activity.
"We found that HCV specifically relies on one DGAT enzymes, DGAT1. Whe we inhibit DGAT1 with a drug, the liver still produces fat droplets through another DGAT enzyme but these droplets cannot be used by HCV," said lead author Eva Herker.hey found that DGAT1 interacts with one viral protein, the viral nucleocapsid core protein, required for viral particle assembly.
The core protein normally associates with the surface of fat droplets but cannot do so when DGAT1 is inhibited or missing in infected cells.
The study was published in the journal Nature Medicine.
Source-ANI
Read more: Hepatitis C Virus Infection Contributed by Liver's Fat Enzyme http://www.medindia.net/news/Hepatitis-C-Virus-Infection-Contributed-by-Livers-Fat-Enzyme-75290-1.htm#ixzz12CpPRtCh
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