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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 virus can reactivate and begin producing large amounts of viral progeny (the lytic part of the viral life cycle) without the host becoming reinfected by new outside virus, and stays within the host indefinitely. [2] Virus latency is not to be confused with clinical latency during the incubation period when a virus is not dormant.
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.
Reactivation of latent viruses has been implicated in a number of diseases (e.g. shingles, pityriasis rosea). Following activation, transcription of viral genes transitions from LAT to multiple lytic genes; these lead to enhanced replication and virus production. Often, lytic activation leads to cell death.
When influenza viruses are inactivated by UV irradiation or ionizing radiation, they remain capable of multiplicity reactivation in infected host cells. [5] [6] [7] If any of a virus's genome segments is damaged in such a way as to prevent replication or expression of an essential gene, the virus is inviable when it, alone, infects a host cell (single infection).
When a cytocidal virus infects a permissive cell, the viruses kill the host cell through changes in cell morphology, in cell physiology, and the biosynthetic events that follow. These changes are necessary for efficient virus replication but at the expense of the host cell.
After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks. In an outbreak, the virus in a nerve cell becomes active and is transported via the neuron's axon to the skin, where virus replication and shedding occur and may cause new sores. [8]
(A) When the host cell is only infected by a giant virus, the latter establishes a cytoplasmic virus factory to replicate and generates new virions, and the host cell is most likely lysed at the end of its replication cycle. (B) When the host cell is co-infected with a giant virus and its virophage, the latter parasitizes the giant virus factory.