In "Swiss Cohort Study" it has been shown that  HIV patient less likely to achieve CD4 cell increases on HAART when co infected with HCV...

Thanks for you kind reply. It might give a clue that HIV patients will be in a poor health condition once coinfected with HCV. But my confusion still existed: for HIV high risk populations with HCV infection at first (eg. negative partners of HIV serodiscordant couples), are they more susceptible to acquire HIV than those without HCV infection? I  didn't find any information about that. I'm not sure whether it is meaningless to do this kind of research or just due to lack of information at present.

HCV does not increase susceptibility to HIV infection per se but they share some commonality in their routes of transmission. So HCV infected populations have a higher risk of also having HIV but this is behavioural rather than the biology of the virus

I hope someone gives you an informed answer. I know that the risk of acquiring HIV infection is increased in those MSM, who have pre-existing bacterial NGU (including chlamydia and trichomoniasis), HPV, and ulcerative STIs such as HSV ulcer or chancre. I do not know about HCV or whether such evidence is now strong, but do believe we jump to conclusions too quickly to claim "all STDs make a person more susceptible". This might not be true, see the answer by Kevin Whitby above. Check "STI and suceptibility to HIV". If you find the answer on your own, please share. I cited some articles in my articles that were focusing on this, but there was never any solid evidence and I do not think HCV was specifically mentioned. Such things are not easy to study and a final proof of causal association might not be possible. There is just epidemiological co-existence.  

I think no, because we found in Mali in 2013 an epidemiological profile disparité and zero coinfection between HIV and HCV infections (see attached file).

Dear experts, thanks for your excellent comments. Until now my understanding on coinfection of HIV and HCV from the epidemiological literatures are only due to their similar transmission. Researchers do believe that is the frequent high risk behaviors among those coinfection people which cause both HIV and HCV infection. The sharing risk behavior of HIV and HCV is the key point. Then the timing of HIV and HCV infection who came first might not be that important. That's why they only focus on the progression of either disease rather than the susceptibility of infection. However, there should be some biological mechanism to strongly convince us, I think, even there is no relation between HCV infection and suceptibility of getting HIV for individuals. Let's go on this topic, I think it'll be an interesting field to explore.

Hi, dear all. I've just got a stimulating answer from a noted epidemiologist of HIV prevention. Except sharing similar high risk behaviors of these two diseases, we should also think about the immune response. Once you get infected with HCV, the immune response will be activated. An activated immune system gives the virus more cells to infect, not only HCV but also other viruses like HIV, which can cause the individual are much easier to get infected wtih HIV. I'm not quite good at the mechanism of biology, but the key point here is the immune response. Hope there's some expert who can help me describe clearly. Thanks!

If there is a preexisting defect in cellular immunity  and HCV is acquired , then the immunologic control  of HCV infection takes  a different course . [ Taylor et al . Clin Infect Dis. 2012 Jul 15; 55(Suppl 1): S33–S42].

In that case , if the immune  response is lowered , ( assuming that this is the different course )  , then ,  maybe the chance of getting infected with HIV becomes higher , considering the similarities in their routes of transmission . 

Thanks for the sharing paper from  Anuradha Sharma. I strongly recommend others to read it. I have to admit that this paper is an excellent one, which definitely enhanced my understanding of HCV and HIV/HCV coinfection a lot. Let me copy some more useful points impressed me from it:

1. HCV infection does not follow the same heterosexual sexual transmission patterns as classic STDs, such as gonorrhea and chlamydial infection. However, certain behaviors, such as anal intercourse and group sex, could result in HCV transmission among heterosexuals.

2. From the Women’s Interagency HIV Study (WIHS), HIV-infected women may be more susceptible than HIVuninfected women to sexually acquired HCV. It is possible that these women engaged in unreported unprotected anal intercourse associated with mucosal trauma and bleeding and that HIV infection increased their susceptibility to HCV infection.

3. Immunologic control of HCV infection may differ if HCV is acquired when there is a preexisting defect due to orthotopic transplantation, HIV infection like this in cellular immunity.

4. Coinfected individuals with percutaneous exposure are usually infected with HCV before HIV acquisition. This may be part of the rationale for endorsing HCV antibody testing only at the time of HIV diagnosis.

5. All HCV-infected persons should be screened for HIV infection. Most of the US data on HIV testing among HCV infected individuals originates from the Veterans Health Administration (VHA), the largest provider of HIV and HCV care in the United States. The VHA has recommended HIV testing for all HCV-infected patients since 2003.

(Comments: unfortunately, there's still lack of information on how  immune response affect HCV-infected patients to easily get HIV than HCV-uninfected patients).

Still look forward to the reasonable mechanism about that. Thanks for your attention.

Dear sir,

See this link may be useful for you.

Hepatitis C coinfection enhances sensitization of CD4(+) T ...

www.ncbi.nlm.nih.gov/pubmed/22024520Traduire cette page

de C Körner - ‎2011 - ‎Cité 18 fois - ‎Autres articles... increased rates of CD4(+) T-cell apoptosis in HCV-infected HIV-positive patients ... Susceptibility to FasL-induced apoptosis was analysed by incubating isolated ... CONCLUSIONS: Our findings suggest a synergistic mechanism in HIV/HCV ...