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Virus latency (or viral latency) is the ability of a pathogenic virus to lie dormant within a cell, denoted as the lysogenic part of the viral life cycle. [1] A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which ...
Viruses enter host cells using a variety of mechanisms, including the endocytic and non-endocytic routes. [4] They can also fuse at the plasma membrane and can spread within the host via fusion or cell-cell fusion. [5] Viruses attach to proteins on the host cell surface known as cellular receptors or attachment factors to aid entry. [6]
The exon parts of LAT-DNA produce two protein products with repeats that are 17 amino acids long, termed HHV latency-related proteins or LR-ORF1 and LR-ORF2. Little is known about these two proteins ( P17588 and P17589 in HHV-1; K4PBJ5 and Q77CA8 in BHV-1), although the loss of ORF2 in bovine herpesvirus-1 (BHV-1) does appear to interfere with ...
Human Immunodeficiency Virus (HIV) has the capability to enter a latent stage of infection where it exists as a dormant provirus in CD4+ T-cells.Most latently infected cells are resting memory T cells, [1] however a small fraction of latently infected cells isolated from HIV patients are naive CD4 T cells.
Varicella zoster virus (VZV) is a member of the alpha subfamily of herpesviruses and is responsible for the human diseases of the chicken pox and shingles. These viruses have their lytic phase in mucoepithelial cells and are latent in neuronal cells. [6] Unlike HSV 1 and 2, there has not been any LAT found in the VZV latent cells.
Incubation period (also known as the latent period or latency period) is the time elapsed between exposure to a pathogenic organism, a chemical, or radiation, and when symptoms and signs are first apparent. [1]
Virus tropism refers to the virus' preferential site of replication in discrete cell types within an organ. In most cases, tropism is determined by the ability of the viral surface proteins to fuse or bind to surface receptors of specific target cells to establish infection.
The herpes virus can then exit this dormant stage and re-enter the lytic cycle, causing disease symptoms. Thus, while herpes viruses can enter both the lytic and lysogenic cycles, latency allows the virus to survive and evade detection by the immune system due to low viral gene expression. The model organism for studying lysogeny is the lambda ...