Two-step evolution of HIV-1 budding system leading to pandemic in the human population.

The pandemic HIV-1, HIV-1 group M, emerged from a single spillover event of its ancestral lentivirus from a chimpanzee. During human-to-human spread worldwide, HIV-1 diversified into multiple subtypes. Here, our interdisciplinary investigation mainly sheds light on the evolutionary scenario of the viral budding system of HIV-1 subtype C (HIV-1C), a most successfully spread subtype.

Antigenic escape is accelerated by the presence of immunocompromised hosts.

The repeated emergence of SARS-CoV-2 escape mutants from host immunity has obstructed the containment of the current pandemic and poses a serious threat to humanity. Prolonged infection in immunocompromised patients has received increasing attention as a driver of immune escape, and accumulating evidence suggests that viral genomic diversity and emergence of immune-escape mutants are promoted in immunocompromised patients. However, because immunocompromised patients comprise a small proportion of the host population, whether they have a significant impact on antigenic evolution at the population level is unknown.

Antithetic effect of interferon-α on cell-free and cell-to-cell HIV-1 infection.

In HIV-1-infected individuals, transmitted/founder (TF) virus contributes to establish new infection and expands during the acute phase of infection, while chronic control (CC) virus emerges during the chronic phase of infection. TF viruses are more resistant to interferon-alpha (IFN-α)-mediated antiviral effects than CC virus, however, its virological relevance in infected individuals remains unclear. Here we perform an experimental-mathematical investigation and reveal that IFN-α strongly inhibits cell-to-cell infection by CC virus but only weakly affects that by TF virus.

A tissue level atlas of the healthy human virome.

Background: Human-resident microbes can influence both health and disease. Investigating the microbiome using next-generation sequencing technology has revealed examples of mutualism and conflict between microbes and humans. Comparing to bacteria, the viral component of the microbiome (i.

Inherited chromosomally integrated HHV-6 possibly modulates human gene expression.

Approximately, 1% of human population possesses a copy of human herpesvirus 6A and 6B (HHV-6A/B) in the genome. This viral element is referred to as inherited chromosomally integrated HHV-6A/B (iciHHV-6A/B) and is encoded in all of their cells. A recent study revealed that iciHHV-6A/B potentially increases the immune responses against HHV-6.

New World feline APOBEC3 potently controls inter-genus lentiviral transmission.

Background: The apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3; A3) gene family appears only in mammalian genomes. Some A3 proteins can be incorporated into progeny virions and inhibit lentiviral replication. In turn, the lentiviral viral infectivity factor (Vif) counteracts the A3-mediated antiviral effect by degrading A3 proteins.

A naturally occurring feline APOBEC3 variant that loses anti-lentiviral activity by lacking two amino acid residues.

Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) is a mammalian protein that restricts lentiviral replication. Various polymorphisms of mammalian genes have been observed in humans, Old World monkeys and domestic cats; however, the genetic diversity of genes in other mammals remains unaddressed. Here we identify a novel haplotype of the feline gene, an gene that restricts feline immunodeficiency virus (FIV) replication, in a Eurasian lynx ().