ArticleFrontiers in microbiology2025
Comparison of viral phenotype and inflammatory biomarker responses in acute HIV-1 subtype A and C infections.
Article in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: HIV-1 subtype A and subtype C infections have different rates of clinical disease progression, with subtype C infected individuals in the IAVI Protocol C multisite acute infection cohort having a 60% faster CD4 loss compared to subtype A. Methods: In order to investigate whether differences were due to the phenotype of the transmitted founder virus (TFV), or inflammatory cytokines and chemokines, known to drive pathogenesis, we PCR amplified, sequenced and constructed infectious molecular HIV-1 clones from the plasma of 30 acutely infected individuals in Rwanda and Zambia. We next compared the inflammatory plasma cytokine/chemokine profiles of individuals pre- and post-the estimated date of infection of 20 Rwandan individuals infected with subtype A and 34 Zambians infected with subtype C HIV-1. Results: A comparison of the replicative capacity of 14 subtype A and 16 subtype C TFV showed that they had similar replicative capacity (RC) scores. Nevertheless, high TFV RC scores were linked to more rapid CD4 Discussion: Overall, the data presented here argue against TFV RC as the basis for different pathogenic outcomes in the subtypes A and C. Moreover, levels of inflammatory cytokines that might drive disease progression were similar during acute infection indicating that additional studies are required to understand the mechanism underlying differences in disease progression between the two subtypes. For both subtypes, high levels of ITAC during acute HIV-1 infection are linked to rapid disease progression.
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