The generalized replication cycle for standard viruses begins with the absorption of the virus by the host cell. Absorption involves an interaction between the viral particle and the potential host cell. This is often mediated by a viral protein that is recognized by a binding protein located on the surface of the host cell. Whether the host cell recognizes the viral protein often determines whether a particular cell can or cannot function as a host for a particular virus. For example, the hemagglutin protein of the influenza virus, a viral protein found within the lipid envelope of this coated virus, interacts with a receptor found on the surface of the epithelial cells that line the human respiratory tract.
The next step in the virus replication cycle is penetration and, if necessary, the uncoating of the virus in the host cell. With some coated viruses, the envelope membrane fuses directly with the host membrane, allowing movement of nucleocapsid into the cell's cytoplasm. Other coated viruses are brought into the cell using endosomes, small vesicles of cellular membrane that bud inwardly and are used to move materials into the cell. Due to the lower pH environment of the endosome, the virus coat can fuse with the endosomal membrane to gain access to the cell cytoplasm. Naked viruses are sometimes small enough to move without help through the host cellular membrane, while others use the endosome system.
Once inside the cell, the virus takes over the host cell's protein and nucleic acid production, directing it to produce viral proteins and genomes. For many viruses having a DNA genome, the viral nucleic acid is inserted or integrated directly into the host cell's own DNA, that make up the cell's chromosomes. RNA viruses tend to keep the genome independent from the host cell's genetic material. In either case, the host cell is fooled into using the viral genetic material as the instructions for the production of new infectious virions. In order to ensure that new virions will be formed, viruses often have mechanisms that speed up the protein formation of the host cell. Sometimes the mechanism will be specific for increased production of viral proteins, while others speed up all protein formation.
A special method of producing new virions is employed by retroviruses, such as the human immunodeficiency virus (HIV). These viruses carry their genomes as RNA, but upon entry into the host cell a viral enzyme known as reverse transcriptase converts the viral RNA into DNA, and that molecule is integrated into the host genome. The enzyme is called reverse transcriptase because generally genetic information moves from DNA to RNA copies rather than this reverse process. The integrated DNA is known as a provirus and will be replicated when the host cell divides, to be inherited by the two resulting daughter cells.
After production of the viral proteins and genomes by the host cellular machinery, the capsid is assembled around the genetic material and, for some viruses, a maturation step occurs that is necessary for infectivity. Finally, the new virions are released from the cell. Some coated viruses leave the cell by budding and do not cause the death of the host cell. The budding process is how the virus acquires its lipid membrane envelope. Other viruses lyse, or break down, the host cell membrane. Lysis kills the host cell.
Because of the ability of viruses to carry genetic material into and out of a cell during the reproduction cycle, viruses can function as vectors in genetic engineering. This is done by inserting foreign genetic material into viral genomes and allowing the material to be integrated and expressed in bacteria and animal cells. Viral vectors are often the basis for gene therapies that in their simplest form attempt to cure genetic defects by providing non-mutated copies of a damaged gene to an organism.
Michelle L. Johnson M.S., The Gale Group Inc., Gale, Detroit,