Herpes simplex virus type 2 (HSV-2) genital shedding in HSV-2-/HIV-1-co-infected women receiving effective combination antiretroviral therapy.

The dynamics of genital shedding of HSV-2 DNA was assessed in HIV-1-infected women taking combination antiretroviral therapy (cART). HIV-1 RNA, HIV-1 DNA and HSV DNA loads were measured during 12-18 months using frozen plasma, PBMC and cervicovaginal lavage samples from 22 HIV-1-infected women, including 17 women naive for antiretroviral therapy initiating cART and 5 women with virological failure switching to a new regimen. Nineteen (86%) women were HSV-2-seropositive. Among HSV-2-/HIV-1-co-infected women, HIV-1 RNA loads showed a rapid fall from baseline after one month of cART, in parallel in paired plasma and cervicovaginal secretions. In contrast, HIV-1 DNA loads did not show significant variations from baseline up to 18 months of treatment in both systemic and genital compartments. HSV DNA was detected at least once in 12 (63%) of 19 women during follow up: HSV-2 shedding in the genital compartment was observed in 11% of cervicovaginal samples at baseline and in 16% after initiating or switching cART. Cervicovaginal HIV-1 RNA loads were strongly associated with plasma HIV-1 RNA loads over time, but not with cervicovaginal HSV DNA loads. Reactivation of genital HSV-2 replication frequently occurred despite effective cART in HSV-2-/HIV-1-co-infected women. Genital HSV-2 replication under cART does not influence cervicovaginal HIV-1 RNA or DNA shedding.

IL28B polymorphism -- predictive factor of HCV infected genotype 1 individuals to treatment response and management of therapy.

It is estimated that approximately 3% of the world population are chronically infected with HCV, as the annual incidence of HCV infection is approximately 3-4 million people. Despite all efforts made to eradicate the HCV infection, after the standard therapy (PegIFN and ribavirin for 48 weeks) only 40-50% of the HCV infected individuals with genotype 1 achieve sustained virological response (SVR). Since our goal today is the eradication of HCV infection, our prior concern has become the identification of predictor factors concerning treatment response. Recent studies such as GWAS have been concerned with the genetic factors and the response to treatment. Recently all interest has been turned towards the demonstration of the host polymorphism located upstream of the IL-28B gene and which is associated with sustained virological response to treatment with pegylated interferon Alfa in combination with ribavirin. Although 2011 comes with the FDA approval of the new triple therapy associating telaprevir/ boceprevir to the standard therapy, a new ethical concern regarding the high costs of this treatment rises the problem of who is the first in line? This is just the beginning of a new quest to further investigate the relationship between the host's polymorphism of the IL-28 gene and the standard and triple therapy in HCV infected individuals in achieving SVR as well as who should receive standard or triple therapy. Determination of the IL-28 polymorphisms may be used together with clinical assessment in order to evaluate patients and to personalize their treatment. The purpose of this paper is to underline the main concerns regarding the goal and endpoints of the HCV therapy, and the relationship of IL-28 in achieving sustained virological response, as well as in pointing out the importance to determine prior to initiating treatment the polymorphism of IL-28 since it is a strong predictor. This is important because it will increase the chances to achieve SVR, it will be cost-effective and reduces adverse effects.