Penetration of virus

Viral infection involves the incorporation of viral DNA into a host cell, replication of that material, and the release of the new viruses. A virus must use cell processes to replicate. The viral replication cycle can produce dramatic biochemical and structural changes in the host cell, which may cause cell damage. These changes, called cytopathic causing cell damage effects, can change cell functions or even destroy the cell. The symptoms of viral diseases result from the immune response to the virus, which attempts to control and eliminate the virus from the body and from cell damage caused by the virus. Many animal viruses, such as HIV Human Immunodeficiency Virus , leave the infected cells of the immune system by a process known as budding, where virions leave the cell individually.

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Influenza A virus surface proteins are organized to help penetrate host mucus

System Penetration | How Malware Penetrates Systems | Kaspersky

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. A virus floating around an enclosed space with possible host cells faces a large hurdle, the thermodynamics of diffusion. Because neutrally charged objects do not naturally clump around each other, the virus must find a way to move even near a host cell. It does this by attachment - or adsorption - onto a susceptible cell; a cell which holds a receptor that the virus can bind to. The receptors on the viral envelope effectively become connected to complementary receptors on the cell membrane. This attachment causes the two membranes to remain in mutual proximity, favoring further interactions between surface proteins.
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MECHANISM OF CELL WALL PENETRATION BY VIRUSES

Author s : John E. Johnson , Manidipa Banerjee. DOI : Host cell entry by influenza and other enveloped viruses is well characterized, however, the manner in which non-enveloped viruses deliver their genome across host cell membranes in the absence of membrane fusion remains unresolved.
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The virus-induced leakage of host-cell constituents represents a true increase in cellular permeability rather than an unpeeling of cell surface components, since an intracellular enzyme participates in the leakage. All of the T-system bacteriophages exhibit this leakage. The leakage does not occur with salt concentrations which permit only reversible virus-cell attachment but no penetration.
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