Abstract
Papillomaviruses (PVs) are a numerous family of small dsDNA viruses infecting virtually all mammals. PVs cause infections without triggering a strong immune response, and natural infection provides only limited protection against reinfection. Most PVs are part and parcel of the skin microbiota. In some cases, infections by certain PVs take diverse clinical presentations from highly productive self-limited warts to invasive cancers. We propose PVs as an excellent model system to study the evolutionary interactions between the immune system and pathogens causing chronic infections: genotypically, PVs are very diverse, with hundreds of different genotypes infecting skin and mucosa; phenotypically, they display extremely broad gradients and trade-offs between key phenotypic traits, namely productivity, immunogenicity, prevalence, oncogenicity and clinical presentation. Public health interventions have been launched to decrease the burden of PV-associated cancers, including massive vaccination against the most oncogenic human PVs, as well as systematic screening for PV chronic anogenital infections. Anti-PVs vaccines elicit protection against infection, induce cross-protection against closely related viruses and result in herd immunity. However, our knowledge on the ecological and intrapatient dynamics of PV infections remains fragmentary. We still need to understand how the novel anthropogenic selection pressures posed by vaccination and screening will affect viral circulation and epidemiology. We present here an overview of PV evolution and the connection between PV genotypes and the phenotypic, clinical manifestations of the diseases they cause. This differential link between viral evolution and the gradient cancer-warts-asymptomatic infections makes PVs a privileged playground for evolutionary medicine research.
Highlights
PV genome structurePapillomaviridae are a diverse family of small, nonencapsulated viruses that infect warm-blooded vertebrates
The conserved elements shared by all PV members are the presence of an upstream regulatory region (URR), the early proteins E1 and E2 and the late proteins L1 and L2 [2]
The best-studied PV is HPV16, a mucosotropic PV that is the primary cause of cervical cancer and of other anogenital cancers [4]
Summary
Papillomaviridae are a diverse family of small, nonencapsulated viruses that infect warm-blooded vertebrates. Virtually all humans are simultaneously colonized by several PVs, causing asymptomatic infections in skin and mucosa. Most likely, this is the case for all other mammals. Cancers associated to chronic infections by a few oncogenic PVs are a major public health concern. Large screening programs for early detection of gynaecological chronic infections by oncogenic PVs were launched decades ago and are being complemented by systematic vaccination programs in the last years. This article aims to bridge the current gap between mechanistic and clinical research on the one hand and evolutionary and ecological research on the other hand, for PVs and the associated infections and diseases
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