Every human suffers through life a number of papillomaviruses (PVs) infections, most of them asymptomatic. A notable exception are persistent infections by Human papillomavirus 16 (HPV16), the most oncogenic infectious agent for humans and responsible for most infection-driven anogenital cancers. Oncogenic potential is not homogeneous among HPV16 lineages, and genetic variation within HPV16 exhibits some geographic structure. However, an in-depth analysis of the HPV16 evolutionary history was still wanting. We have analyzed extant HPV16 diversity and compared the evolutionary and phylogeographical patterns of humans and of HPV16. We show that codivergence with modern humans explains at most 30% of the present viral geographical distribution. The most explanatory scenario suggests that ancestral HPV16 already infected ancestral human populations and that viral lineages co-diverged with the hosts in parallel with the split between archaic Neanderthal-Denisovans and ancestral modern human populations, generating the ancestral HPV16A and HPV16BCD viral lineages, respectively. We propose that after out-of-Africa migration of modern human ancestors, sexual transmission between human populations introduced HPV16A into modern human ancestor populations. We hypothesize that differential coevolution of HPV16 lineages with different but closely related ancestral human populations and subsequent host-switch events in parallel with introgression of archaic alleles into the genomes of modern human ancestors may be largely responsible for the present-day differential prevalence and association with cancers for HPV16 variants.

Invasive cervical cancer disproportionately affects women without sufficient access to care, with higher rates among minority groups in higher-income countries and women in low-resource regions of the world. Many elements contribute to racial/ethnic disparities in the cervical cancer continuum - from screening and diagnosis to treatment and outcome. Sociodemographic factors, access to healthcare, income and education level, and disease stage at diagnosis are closely linked to such inequities. Despite the identification of such elements, racial/ethnic disparities persist, and are widening in several minority subgroups, particularly in older women, who are ineligible for human papillomavirus (HPV) vaccination and are underscreened. Recent studies suggest that racial/ethnic differences in HPV infection exist and may also have a role in observed differences in cervical cancer. In this review, we provide an overview of the current literature on racial disparities in cervical cancer screening, incidence, treatment and outcome to inform future strategies to reduce persistent inequities.

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HIV-1 B is predominant in Brazil, but HIV-1 C has increasingly been reported in the south of the country. However, many samples clustering with clade C are actually a recombinant, with a small B segment at RT (CRF31). Samples (209) from the three cities with the highest aids prevalence rate are analyzed. Partial polymerase sequences from HIV RNA made it possible to determine HIV clades and recombination patterns and to identify primary drug resistance mutations (DRMs). The incidence was estimated with a BED assay. HIV-1 C and CRF31 patterns were twice as frequent as clade B at all sites, but the proportion of C and CRF31 patterns was significantly different among sites. The incidence estimate for SC was 2.6 persons-years. Infection in recent or younger cases showed no association with clade C. Surveillance DRM was observed in 8.3% (95% CI 5-13), mostly to NNRTIs. Clade F pol genomes had significantly more primary DRM.