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Viral entry is the earliest stage of infection in the viral life cycle, as the virus comes into contact with the host cell and introduces viral material into the cell. The major steps involved in viral entry are shown below. [1] Despite the variation among viruses, there are several shared generalities concerning viral entry. [2]
To enter the cells, proteins on the surface of the virus interact with proteins of the cell. Attachment, or adsorption, occurs between the viral particle and the host cell membrane. A hole forms in the cell membrane, then the virus particle or its genetic contents are released into the host cell, where replication of the viral genome may commence.
Entry, or penetration, is the second step in viral replication. This step is characterized by the virus passing through the plasma membrane of the host cell. The most common way a virus gains entry to the host cell is by receptor-mediated endocytosis, which comes at no energy cost to the virus, only the host cell. Receptor-mediated endocytosis ...
In the lytic cycle, the viral DNA exists as a separate free floating molecule within the bacterial cell, and replicates separately from the host bacterial DNA, whereas in the lysogenic cycle, the viral DNA is integrated into the host genome. This is the key difference between the lytic and lysogenic cycles.
Other viruses utilize host cell proteins to shield viral DNA until it has reached the nucleus. Upon entry into the host cell cytoplasm, the HIV-1 capsid is recognized and bound by cyclophilin A (CypA); this affinity interaction stabilizes the capsid and prevents exposure of the HIV-1 cDNA to pattern recognition receptors in the cytoplasm.
The viral particle is about 30 nm in diameter with icosahedral symmetry. Because of its short genome and its simple composition—only a strand of RNA and a nonenveloped icosahedral protein coat encapsulating it—poliovirus is widely regarded as the simplest significant virus.
A viral infection does not always cause disease. A viral infection simply involves viral replication in the host, but disease is the damage caused by viral multiplication. [5] An individual who has a viral infection but does not display disease symptoms is known as a carrier. [17] Mechanisms by which viruses cause damage and disease to host cells
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 ...