BACKGROUND: The occurrence of human immunodeficiency virus type 1 (HIV-1) superinfection has implications for vaccine development and our understanding of HIV pathogenesis and transmission. METHODS AND RESULTS: We describe a subject from the Multicenter AIDS Cohort Study who was superinfected with a dual-tropic (CXCR4/CCR5-utilizing) HIV-1 subtype B strain between 0.8 and 1.3 years after seroconversion who had rapid progression to AIDS; the subject developed Pneumocystis pneumonia 3.4 years after seroconversion, as well as multiple other opportunistic infections. The superinfecting strain rapidly became the predominant population virus, suggesting that the initial and superinfecting viruses in this individual differed in virulence. However, we found no molecular epidemiological evidence in the HIV database to suggest that this strain had been found in other individuals. In addition, this subject's HIV-1 viral load and pattern of human leukocyte antigen and coreceptor polymorphisms only partially explained his rapid disease progression. CONCLUSIONS: Additional studies are needed to determine whether superinfection itself and/or infection with a dual-tropic virus causes rapid disease progression, or whether certain individuals who are innately more susceptible to rapid disease progression also lack the ability to resist the challenge of a second infection. This case appears to support the latter hypothesis.
BACKGROUND: The occurrence of humanimmunodeficiency virus type 1 (HIV-1) superinfection has implications for vaccine development and our understanding of HIV pathogenesis and transmission. METHODS AND RESULTS: We describe a subject from the Multicenter AIDS Cohort Study who was superinfected with a dual-tropic (CXCR4/CCR5-utilizing) HIV-1 subtype B strain between 0.8 and 1.3 years after seroconversion who had rapid progression to AIDS; the subject developed Pneumocystis pneumonia 3.4 years after seroconversion, as well as multiple other opportunistic infections. The superinfecting strain rapidly became the predominant population virus, suggesting that the initial and superinfecting viruses in this individual differed in virulence. However, we found no molecular epidemiological evidence in the HIV database to suggest that this strain had been found in other individuals. In addition, this subject's HIV-1 viral load and pattern of human leukocyte antigen and coreceptor polymorphisms only partially explained his rapid disease progression. CONCLUSIONS: Additional studies are needed to determine whether superinfection itself and/or infection with a dual-tropic virus causes rapid disease progression, or whether certain individuals who are innately more susceptible to rapid disease progression also lack the ability to resist the challenge of a second infection. This case appears to support the latter hypothesis.
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