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Italian Seroconversion Study

Publications and source records attributed to Italian Seroconversion Study.

6 recordsLinked to original sources
PubMed2005

Changes over time in post-seroconversion CD4 cell counts in the Italian HIV-Seroconversion Study: 1985-2002.

OBJECTIVE: To determine whether there has been a tendency for early post-seroconversion CD4 cell counts to change over calendar time. DESIGN: A prospective cohort study of individuals with well-estimated dates of seroconversion. METHODS: We studied 1251 individuals who seroconverted to HIV in Italy between 1985 and 2002, and for whom the first CD4 count was measured within 2 years of seroconversion and before any use of antiretrovirals. Linear regression models were used to assess evidence for a trend in post-seroconversion CD4 cell count over time. RESULTS: The median post-seroconversion CD4 cell count was 674 x 10 cells/l in those seroconverting between 1985 and 1990, 588 x 10 cells/l for 1991 to 1994, 559 x 10 cells/l for 1995 to 1998 and 494 x 10 cells/l for 1999 to 2002. The post-seroconversion CD4 cell count decreased by an average of 8.4 x 10 cells/l per year (95% confidence interval, 4.0-12.9; P < 0.001), after adjustment for potential confounders, including interval between HIV-negative and HIV-positive tests, lag time for first CD4 cell count measurement, age at seroconversion, gender, HIV-transmission group, and clinical centre. The finding was consistent in sensitivity analyses restricted to those with information on acute infection. CONCLUSION: These data suggest a possible decreasing trend in CD4 cell count immediately following seroconversion in Italy which requires further investigation.

AIDS-Related Opportunistic Infections↗
PubMed2003

Effect of multiple herpesvirus infections on the progression of HIV disease in a cohort of HIV seroconverters.

The effects of herpesviruses infection on the progression of HIV disease remain controversial, with some studies showing accelerated progression and others showing no effect. Furthermore, the effect of concurrent infection with more than one herpesvirus on the progression of HIV disease has never been investigated. To this end, the rates of progression of HIV disease were determined after stratifying for the presence of up to five different herpesvirus infections. The study population consisted of 359 HIV-infected persons for whom the date of seroconversion was estimated (part of the Italian Seroconversion Study). One serum sample from each participant was tested for antibodies to five herpesviruses: HSV-2, CMV, HHV-6, HHV-7, and HHV-8. Univariate analysis showed that HSV-2 and HHV-8 were significantly associated with progression to AIDS, yet when adjusting for age at HIV seroconversion and for the presence of the other herpesvirus infections, only HHV-8 infection showed a significant association. The age-adjusted risk of progression to AIDS with Kaposi's sarcoma increased with the number of herpesvirus infections and was significant in individuals with four infections. The risk of progression to AIDS without Kaposi's sarcoma also increased with the number of infections, although not significantly. Similar results were found when considering CD4+ cell count <200 x 10(6) cells/L as the endpoint. Concurrent infection with more than one herpesvirus does not appear to have a significant effect on the course of HIV disease, except for the known association between HHV-8 and Kaposi's sarcoma. However, even after excluding Kaposi's sarcoma from the AIDS-defining endpoints, a slightly increased risk for participants with four herpesvirus infections remained.

AIDS-Related Opportunistic Infections↗
PubMed2002

No protective effect of acyclovir on HIV disease progression in a cohort of HSV-2-HIV-infected individuals.

The efficacy of anti-herpetic drugs in decreasing HIV disease progression has not been clarified. We studied a cohort of 126 HIV-positive individuals with known date of seroconversion who were HSV-2-seropositive to determine if progression to AIDS was influenced by treatment with acyclovir. In the multivariate analysis, being homosexual and low CD4 count were associated with a faster progression to AIDS, whereas treatment with acyclovir showed a 37.0% protective effect compared to those who did not receive it when antiretroviral treatment was not included in the model. When including antiretroviral therapy, the protective effect of acyclovir decreased to 9.0% and that of antiretroviral therapy was 43.0% for monotherapy and 36.0% for double therapy, suggesting that most of the protective effect of acyclovir in the previous model was due to antiretroviral therapy. In conclusion, treatment with acyclovir does not seem to prolong significantly survival to AIDS among HIV-positive individuals who are HSV-2-infected.

Acyclovir↗
PubMed2001

Response to highly active antiretroviral therapy according to duration of HIV infection.

OBJECTIVE: To evaluate whether duration of HIV-1 infection influences the response to highly active antiretroviral therapy (HAART). DESIGN: Prospective study of individuals (Italian Seroconversion Study cohort) with well-estimated dates of HIV-1 seroconversion. METHODS: This analysis included 277 participants who began HAART (defined as three antiretroviral drugs used in combination). Cox regression models were used to evaluate the association between duration of infection (as categorical variable [</=3, 3-7.5, >7.5 years from seroconversion] or continuous variable) and an immunologic (rise in CD4 count >100 cells/mm3) and a virologic (decline in plasma HIV-RNA to unquantifiable levels) outcome. All analyses were stratified by center of recruitment and adjustment, when used, was for gender, age at inception of HAART, injection drug use, previous antiretroviral therapy, lag-time between positive and negative HIV test result, year of starting HAART, clinical stage, CD4 count, and HIV-RNA at time of HAART. RESULTS: HAART was initiated a median of 6.4 years after seroconversion. There was a median follow-up of 1.6 years after starting HAART to the calendar cut-off (November 1999). One-hundred-eighty-one (65.3%) patients experienced a decline in viral load to below quantifiable levels and 184 (66.4%) experienced a rise in CD4 >100 cells/mm3. In the Cox models, by 1-year increase in duration of infection, we estimated a lower crude hazard of achieving a CD4 count increase >100 cells (relative hazard [RH], 0.96; 95% confidence interval [CI], 0.92-1.01; p =.09), and a lower hazard of reaching an unquantifiable level of plasma HIV-RNA (RH, 0.97; 95%CI, 0.93-1.02; p =.20). After adjustment, these values became 0.99 (95%CI, 0.93-1.04; p =.62) and 0.98 (95%CI, 0.93-1.04; p =.48), respectively. When duration of HIV infection was considered as a categorical variable, the results were consistent with those already described. CONCLUSIONS: These results suggest that the duration of HIV infection does not seem to play an important independent role in determining the virologic and immunologic responses to HAART.

Adult↗