Related papers: Deleterious synonymous mutations hitchhike to high…
Human immunodeficiency virus (HIV-1 or simply HIV) induces a persistent infection, which in the absence of treatment leads to AIDS and death in almost all infected individuals. HIV infection elicits a vigorous immune response starting about…
During chronic infection, HIV-1 engages in a rapid coevolutionary arms race with the host's adaptive immune system. While it is clear that HIV exerts strong selection on the adaptive immune system, the characteristics of the somatic…
The rates of escape and reversion in response to selection pressure arising from the host immune system, notably the cytotoxic T-lymphocyte (CTL) response, are key factors determining the evolution of HIV. Existing methods for estimating…
In early HIV infection, the virus population escapes from multiple CD8+ cell responses. The later an escape mutation emerges, the slower it outgrows its competition, i. e. the escape rate is lower. This pattern could indicate that the…
Mutation rates and fitness costs of deleterious mutations are difficult to measure in vivo but essential for a quantitative understanding of evolution. Using whole genome deep sequencing data from longitudinal samples during untreated HIV-1…
Following transmission, HIV-1 evolves into a diverse population, and next generation sequencing enables us to detect variants occurring at low frequencies. Studying viral evolution at the level of whole genomes was hitherto not possible…
Many microbial populations rapidly adapt to changing environments with multiple variants competing for survival. To quantify such complex evolutionary dynamics in vivo, time resolved and genome wide data including rare variants are…
Chronic infections of the human immunodeficiency virus (HIV) create a very complex co-evolutionary process, where the virus tries to escape the continuously adapting host immune system. Quantitative details of this process are largely…
Cytotoxic T-lymphocytes (CTLs) recognize viral protein fragments displayed by major histocompatibility complex (MHC) molecules on the surface of virally infected cells and generate an anti-viral response that can kill the infected cells.…
The evolution of drug resistance in HIV occurs by the fixation of specific, well-known, drug-resistance mutations, but the underlying population genetic processes are not well understood. By analyzing within-patient longitudinal sequence…
During an infection, HIV experiences strong selection by immune system T cells. Recent experimental work has shown that MHC escape mutations form an important pathway for HIV to avoid such selection. In this paper, we study a model of MHC…
A survey of the patterns of synonymous codon preferences in the HIV env gene reveals a relation between the codon bias and the mutability requirements in different regions in the protein. At hypervariable regions in $gp120$, one finds a…
The evolutionary dynamics of HIV during the chronic phase of infection is driven by the host immune response and by selective pressures exerted through drug treatment. To understand and model the evolution of HIV quantitatively, the…
Although several synonymous codons can encode the same aminoacid, this symmetry is generally broken in natural genetic systems. In this article, we show that the symmetry breaking can result from selective pressures due to the violation of…
One way in which the human immunodeficiency virus (HIV-1) replicates within a host is by infecting activated CD4+ T-cells, which then produce additional copies of the virus. Even with the introduction of antiretroviral drug therapy, which…
The vertebrate adaptive immune system provides a flexible and diverse set of molecules to neutralize pathogens. Yet, viruses such as HIV can cause chronic infections by evolving as quickly as the adaptive immune system, forming an…
The twin processes of viral evolutionary escape and reversion in response to host immune pressure, in particular the cytotoxic T-lymphocyte (CTL) response, shape Human Immunodeficiency Virus-1 sequence evolution in infected host…
Broadly neutralizing antibodies are promising candidates for treatment and prevention of HIV-1 infections. Such antibodies can temporarily suppress viral load in infected individuals; however, the virus often rebounds by escape mutants that…
In this paper, we propose a mathematical model for HIV-1 infection with intracellular delay. The model examines a viral-therapy for controlling infections through recombining HIV-1 virus with a genetically modified virus. For this model,…
We construct a seven-component model of the in-host dynamics of the Human Immunodeficiency Virus Type-1 (i.e, HIV) that accounts for latent infection and the propensity of viral mutation. A dynamical analysis is conducted and a theorem is…