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Rapid Disease Progression in Human Immunodeficiency Virus Type 1-Infected Seroconverters in India
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Updated: 2005-11-23 01:16:31
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Your Name: B.Vilasini
URL: http://www.nari-icmr.res.in/2002_5.pdf  (Text Version)
A gist of the contents at the URL: Rapid Disease Progression in Human Immunodeficiency Virus Type 1-Infected Seroconverters in India.

Sanjay M. Mehendale, Robert C. Bollinger, Smita S. Kulkarni,
Rebecca Y. Stallings, Ronald S. Brookmeyer, Sangita V. Kulkarni,
Anand D. Divekar, Raman R. Gangakhedkar, Smita N. Joshi, Arun R. Risbud,
Madhuri A. Thakar, Bharati A. Mahajan, Varsha A. Kale, Manisha V. Ghate,
Deepak A. Gadkari, Thomas C. Quinn and Ramesh S. Paranjape.
AIDS RESEARCH AND HUMAN RETROVIRUSES
2002, Volume 18, Number 16, , pp.1175–1179.


ABSTRACT

To determine if the early immunological and virological events of HIV infection are unique in a setting with limited access to health care and HIV-1 subtype C infection, we undertook a prospective cohort study to characterize the early natural history of HIV viral load and CD41 T lymphocyte counts in individuals with recent HIV seroconversion in India. CD41 T lymphocyte counts were prospectively measured for up to 720 days in 46 antiviral drug-naive persons with very early HIV infection,documented by HIV antibody seroconversion.HIV viral RNA levels were measured subsequently on reposited plasma samples from these same time points. The median viral load “set point” for Indian seroconverters was 28,729 RNA copies/ml. The median CD41 cell count following acute primary HIV infection was 644 cells/mm3. Over the first 2 years since primary infection, the annual rate of increase in HIV viral load was 18274 RNA copies/ml/year and the annual decline in CD4 cell count was 2120 cells/year. Although the viral “set point” was similar, the median trajectory of increasing viral load in Indian seroconverters was greater than what has been reported in untreated
HIV seroconverters in the United States. These data suggest that the more rapid HIV disease progression described
in resource-poor settings may be due to very early virological and host events following primary HIV infection. A rapid increase in viral load within the first 2 years after primary infection may have to be considered when applying treatment guidelines for antiretroviral therapy and opportunistic infection prophylaxis.
 
 
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