Like bacteriophages, some animal viruses use DNA while others use RNA molecules to carry their genetic information. Virus particles often termed virions are assembled through two strategies. The simplest strategy involves wrapping the viral genome in a protein coat or capsid. Without exception the capsid proteins are encoded by the viral genome
A more complex strategy for constructing a virion is used by the majority of animal cell viruses. As above, their genomic DNA or RNA is wrapped in a protein coat. This protein coat, nucleic acid complex (sometimes called a nucleocapsid ), is then wrapped in a second outer coat a lipid membrane. The lipid membrane is usually acquired as the viral nucleocapsid exits the host cell. As it is being pushed though the host plasma membrane a patch of this membrane becomes wrapped around the nucleocapsid. Hence the membraneous outer layer of the virion is of host cell origin.
A wide variety of animal cell viruses use this membrane-scavenging strategy for forming their virions. Among these are the influenza virus, encephalitis virus smallpox virus, rabies virus, herpes virus and the human immunodeficiency virus (HIV) In each case, the membrane surrounding nucleocapsid is studded with an array of virus-encoded proteins. Usually the N- termini of these proteins protrude outward into the fluid outside of the viral particle; the C- termini often contact the nucleocapsid inside the membrane. Since lipid bilayers are easily dissolved by detergents these lipid-containing virions are readily inactivated by soaps and detergents while the purely proteinaceous virions are quite resistant to soaps
This explains why most gastrointestinal viruses (including poliovirus) have virions that are purely protein. Their virions can resist the strong detergents present in the liver bile that is constantly introduced into the small intestine to aid with digestion. Lipid containing virions are inactivated by the bile and cannot infect cells further down in the intestine
All virus capsids whether purely protein or protein:lipid composites share two traits: they must protect the nucleic acid inside from substances that might destroy the viral genome and they must facilitate the adsorption (attachment) of the virion to the surface of the host cell. The invasion of a cell by a virus particle always depends upon a specific and tight binding of the virus particle to some surface component of the host cell's plasma membrane.
Viruses have evolved the means to recognize and bind tightly to cell proteins. Invariably these tethering sites on the host cell are normal cell proteins. Each type of virus takes advantage of different proteins to gain entry to a specific type of host cell. In the case of purely proteinaceous capsids the capsid proteins have affinity for one or another of the host cell's surface molecules; in the case of lipid-containing virions the viral proteins extending from the membrane can attach to a host cell surface protein
This adsorption must be followed by penetration where the virus succeeds in crossing the plasma membrane and entering the cytoplasm of the host cell. Since the host cell is constantly internalizing its own membrane proteins and recycling them back to the surface many viruses hitch a ride on these host cell proteins to gain entrance into the cell. Other viruses, including HIV have developed the means to fuse themselves to the host cell thereby allowing the nucleocapsid direct access to the host cell interior. Once inside some viruses complete their entire replication cycle inside the cytoplasm yet others may move into the nucleus to replicate
A more complex strategy for constructing a virion is used by the majority of animal cell viruses. As above, their genomic DNA or RNA is wrapped in a protein coat. This protein coat, nucleic acid complex (sometimes called a nucleocapsid ), is then wrapped in a second outer coat a lipid membrane. The lipid membrane is usually acquired as the viral nucleocapsid exits the host cell. As it is being pushed though the host plasma membrane a patch of this membrane becomes wrapped around the nucleocapsid. Hence the membraneous outer layer of the virion is of host cell origin.
A wide variety of animal cell viruses use this membrane-scavenging strategy for forming their virions. Among these are the influenza virus, encephalitis virus smallpox virus, rabies virus, herpes virus and the human immunodeficiency virus (HIV) In each case, the membrane surrounding nucleocapsid is studded with an array of virus-encoded proteins. Usually the N- termini of these proteins protrude outward into the fluid outside of the viral particle; the C- termini often contact the nucleocapsid inside the membrane. Since lipid bilayers are easily dissolved by detergents these lipid-containing virions are readily inactivated by soaps and detergents while the purely proteinaceous virions are quite resistant to soaps
This explains why most gastrointestinal viruses (including poliovirus) have virions that are purely protein. Their virions can resist the strong detergents present in the liver bile that is constantly introduced into the small intestine to aid with digestion. Lipid containing virions are inactivated by the bile and cannot infect cells further down in the intestine
All virus capsids whether purely protein or protein:lipid composites share two traits: they must protect the nucleic acid inside from substances that might destroy the viral genome and they must facilitate the adsorption (attachment) of the virion to the surface of the host cell. The invasion of a cell by a virus particle always depends upon a specific and tight binding of the virus particle to some surface component of the host cell's plasma membrane.
Viruses have evolved the means to recognize and bind tightly to cell proteins. Invariably these tethering sites on the host cell are normal cell proteins. Each type of virus takes advantage of different proteins to gain entry to a specific type of host cell. In the case of purely proteinaceous capsids the capsid proteins have affinity for one or another of the host cell's surface molecules; in the case of lipid-containing virions the viral proteins extending from the membrane can attach to a host cell surface protein
This adsorption must be followed by penetration where the virus succeeds in crossing the plasma membrane and entering the cytoplasm of the host cell. Since the host cell is constantly internalizing its own membrane proteins and recycling them back to the surface many viruses hitch a ride on these host cell proteins to gain entrance into the cell. Other viruses, including HIV have developed the means to fuse themselves to the host cell thereby allowing the nucleocapsid direct access to the host cell interior. Once inside some viruses complete their entire replication cycle inside the cytoplasm yet others may move into the nucleus to replicate