Most people infected with hepatitis C virus (HCV) do not have any acute signs or symptoms of hepatitis. They usually remain unaware that they have been infected during the first 10‐20 years, unless they have a blood test. They will usually be found to have some elevations of liver enzymes in their blood, as a result of leakage of these enzymes from damaged or dying liver cells. Specific blood tests can determine the presence of antibodies to HCV, or measure the blood level of HCV RNA, also known as viral load, by polymerase chain reaction detectable within 45‐90 days.
The precise mechanisms by which HCV infection causes liver damage are not known; however, there is strong evidence that a person’s own immunologic response to HCV contributes significantly to this process. The final outcome of infections by viruses that cause chronic diseases is believed to depend mostly upon the rate of replication of the infecting virus and the capacity of the immune system to mount rapid, multispecific and efficient virusspecific responses to inhibit infection before the virus can devise strategies to evade immune surveillance.
HCV is a single‐stranded RNA virus which does not integrate into the host’s genetic material. HCV must constantly replicate to maintain its presence in the human body and is very efficient at replicating inside of human cells. The clinical significance of extra hepatic HCV is not fully understood, and it is difficult to definitively determine the presence of replication in the absence of an in vivo model.
In a recent publication, Laskus documented evidence of HCV replication in peripheral blood cells (monocytes/macrophages, and T and B cells) in HCV/HIV coinfected patients. He suggests that HCV may replicate in the same cells infected with HIV and that there may be direct interactions between the two viruses. When interferon alfa (IFN) therapy is given to people with HCV infection, there is two‐phase decay. There is an initial rapid decrease in HCV RNA, then a secondary, slower decay, or decrease.
The initial decay, about a 1.5 log decrease in HCV RNA seen during the first 48 hours, is thought to represent the death of HCV‐infected hepatocytes, or liver cells. Studies have shown that neutralizing antibodies are produced during HCV infection, but they do not appear to be protective against re‐infection in humans or in chimpanzees. The more critical determinate of the outcome of HCV infection seems to be the cell‐mediated immune response, or the T‐ Cell (CD4) response.
People who are able to spontaneously clear HCV from their body have evidence of strong T‐cell responses. Conversely, people who are chronically infected with HCV do not appear to either mount a strong T‐cell response early after HCV infection, or maintain an initial strong T‐cell response to HCV antigens. In Gerlach’s study, the 20 people (52.6%) out of 38 studied who cleared HCV infection all had a strong sustained antiviral T‐cell response to HCV, while the people who became chronically infected either showed no initial T‐cell
response (12, 31.6%) or did not maintain an initial strong antiviral T‐cell response (6, 15.8%). Over time, however, in most people chronically infected with HCV, T‐cell responses increase but are not able to clear HCV.
Possible Strategies for a Virus to Escape Immune Elimination
1. Decrease its visibility to the immune system.
2. Decrease the effectiveness of antiviral cytokines.
3. Increase the resistance of infected cells to CTL‐mediated killing.
4. Infect immunologically privileged sites.
5. Induce immunologically tolerance.
6. Immunologic evasion
While HCV is an RNA virus, it is not a retrovirus; therefore, HCV does not incorporate its genetic code into the host cell’s DNA. So if all infected liver cells, or hepatocytes, and any other cells in the body which are infected with HCV die—and there are no free HCV virions around to infect new cells‐then the person will no longer be infected with HCV (i.e., the infection will be eradicated). Some investigators
believe that most people who remain without detectable HCV RBA six months after therapy have achieved eradication (i.e., they are cured). Approximately 15% of people acutely infected with HCV are able to achieve life‐long eradication of HCV from their body by their immune response. Whether people are in fact cured will require longer follow‐up; however, there is an important implication to achieving eradication. People can be re‐infected with HCV after they have had the initial HCV infection eradicated; there is no life‐long HCV immunity.
The nature of the receptors enabling hepatitis C virus (HCV) entry into cells has been the subject of debate. On one hand, ligand panning with recombinant HCV envelope protein has indentified CD81, a member of the tetraspanin superfamily of proteins, as a direct ligand for the E2 glycoprotein. On the other, virus present in infected blood is found associated with low‐density lipoprotein (LDL) and the LDL receptor (LDL‐R) has been suggested as a receptor for the virus. Zhabilov discloses method for isolating and preparing an inactivated pepsin fraction (IPF) useful for detecting and treating HIV1 HCV and some autoimmune and viral diseases. According to preliminary trials the complex antigen of IPF and viral antigens together through alfa 1 alfa 2 and beta serum fractions which form inside the body, blocks contact virus and hepatocytes and immune cells at the same time trigger an immune reaction.
The new antigen complex triggers an immune reaction model
with the participation of T lymphocytes with gamma‐delta chains of their surface. In this way, IPF appears like an immune creator and can be used for treatment of HCV infection. The results of this approach by using IPF SA immune creator that takes part in creating a complex antigen having the properties of a vaccine. The new antigen complex triggers an immune reaction model with the participation of T lymphocytes. The results of the pilot testing study conducted clearly show the action and effectiveness of IPF. Immunological results by Dr. Santos from Centro Medico Nova in Mexico are:
1. Increase in percentage and numbers of CD8 positive cells in the treated patients
2. Significant decline CD8+CD38+cells in treated patients
3. Significant increase in both the CD4+iNFg secreting cells as well as the CD8+iNFg secreting cells
in the treated patients
4. Increase all the cytokines such as IL2 IL6 IL12 relate with the TH1 immune response
All of the above immunological changes show the immunological effect of IPF. The shown
immunological results can open a window for the creation of vaccine treating against viral diseases such
Written by: Harry Zhabilov
President and Chief Science Officer
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V HIV HPV and genital herpes etc…..