One person’s fight against an HIV infection can decrease the virus’s ability to threaten its next victim, say Goepfert et al. (page 1009). Mutations that help the virus survive in one host decrease its ability to replicate in the next. HIV mutations that help the virus bypass the host’s immune system often fall within gag. This gene is a favorite target for mutations because, for some reason, G...

One person’s fight against an HIV infection can decrease the virus’s ability to threaten its next victim, say Goepfert et al. (page 1009). Mutations that help the virus survive in one host decrease its ability to replicate in the next. HIV mutations that help the virus bypass the host’s immune system often fall within gag. This gene is a favorite target for mutations because, for some reason, G...

Mutations in the epitopes of antigenic proteins can confer viral resistance to antibody-mediated neutralization. However, the fundamental properties that characterize epitope residues and how mutations affect antibody binding to alter virus susceptibility to neutralization remain largely unknown. To address these questions, we used an ensemble-based algorithm to characterize the effects of muta...

One person’s fight against an HIV infection can decrease the virus’s ability to threaten its next victim, say Goepfert et al. (page 1009). Mutations that help the virus survive in one host decrease its ability to replicate in the next. HIV mutations that help the virus bypass the host’s immune system often fall within gag. This gene is a favorite target for mutations because, for some reason, G...

Antiviral CD8(+) T cells are a key component of the adaptive immune system against hepatitis C virus (HCV). For the development of immune therapies, it is essential to understand how CD8(+) T cells contribute to clearance of infection and why they fail so often. A mechanism for secondary failure is mutational escape of the virus. However, some substitutions in viral epitopes are associated with...

BACKGROUND Because of the high prevalence and absence of cure for infection, chronic hepatitis B virus (HBV) infection has been acknowledged as a pressing public health issue. Toll-like receptors (TLRs) activate the human innate immune system and the polymorphisms in TLRs may alter their function. The present study aimed to investigate the association between TLR polymorphisms and disease progr...

Mutations in the human hepatitis B virus (HBV) genome contribute to its escape from host immune surveillance and result in persistent infections. The aim of this study was to characterize the molecular variations of the surface gene and protein in chronically-infected patients from the southern part of Iran. The surface genes from 12 HBV chronic carriers were amplified, sequenced and subsequent...

Following transmission, HIV-1 adapts in the new host by acquiring mutations that allow it to escape from the host immune response at multiple epitopes. It also reverts mutations associated with epitopes targeted in the transmitting host but not in the new host. Moreover, escape mutations are often associated with additional compensatory mutations that partially recover fitness costs. It is uncl...

Most experimental studies of epistasis in evolution have focused on adaptive changes-but adaptation accounts for only a portion of total evolutionary change. Are the patterns of epistasis during adaptation representative of evolution more broadly? We address this question by examining a pair of protein homologs, of which only one is subject to a well-defined pressure for adaptive change. Specif...