Conceptually the simplest viruses to understand are those with genomes of double stranded DNA. Once the nucleocapsid of this type of virus enters the cell it proceeds to the nucleus where it mimics the genome of the host cell. Usually the viral genome is replicated using the host cell DNA polymerase and the viral genome is transcribed by the host cell RNA polymerase. The resulting transcripts carrying information encoding viral proteins is then transported to the cytoplasm and seen as a template by the host cell ribosomes. Some of these newly synthesized viral proteins are used as the protein capsid around newly replicated viral DNA molecules. These new virions are released from the cell where they target other host cells and trigger new rounds of infection
The dsDNA viruses that exploit the host cell machinery to complete their life cycles can carry small genomes encoding mostly viral structural proteins like those for the capsid. However the dependence of these viruses on the host cell replication machinery creates a potentially awkward situation the enzymes of DNA replication are generally not expressed in quiescent cells. Most of the cells infected will be in G and therefore inhospitable hosts. Some dsDNA viruses like the herpes virus family or the Epstein Barr virus have large genomes that contain greater than sixty genes.
These viruses encode their own DNA polymerase and thus ensure their ability replicate in quiescent cells. Other viruses circumvent this problem by producing a protein that induces the resting host cell to enter the active cell cycle. This ensures that the host cell replication enzymes are available for exploitation and reproduction of the virus. This means of producing many virions usually results in host cell death
Note however, what may happen if the infected cell is not killed by the virus. The presence of the virus and the viral growth-promoting protein can drive the host cell into unceasing growth and cell division. This converts the host cell growth from a normal pattern to a pattern typical of cancer cells. The gene that encodes the growth-promoting protein can function as an oncogene that acts to transform the infected cell into a cancer cell
More than 90% of human cervical carcinomas are associated with infection by human papilloma virus a dsDNA virus that infects the lining of the cervix. In order for HPV to create a tumor the viral genome must perpetuate itself so when the original infected cell divides into many cells each new cell contains the virus and the viral growth promoting protein
The Epstein Barr dsDNA virus that results in mononucleosis in this country. For reasons that are unclear the Epstein Barr virus triggers Burkitts lymphoma in central Africa and a tumor of the nasal cavity in Southeast Asia. These tumors are inadvertent by products of the need to replicate viral DNA. The outgrowth of tumors happens on occasion when virus infected cells are not eliminated by the completion of the viral lytic cycle
The dsDNA viruses that exploit the host cell machinery to complete their life cycles can carry small genomes encoding mostly viral structural proteins like those for the capsid. However the dependence of these viruses on the host cell replication machinery creates a potentially awkward situation the enzymes of DNA replication are generally not expressed in quiescent cells. Most of the cells infected will be in G and therefore inhospitable hosts. Some dsDNA viruses like the herpes virus family or the Epstein Barr virus have large genomes that contain greater than sixty genes.
These viruses encode their own DNA polymerase and thus ensure their ability replicate in quiescent cells. Other viruses circumvent this problem by producing a protein that induces the resting host cell to enter the active cell cycle. This ensures that the host cell replication enzymes are available for exploitation and reproduction of the virus. This means of producing many virions usually results in host cell death
Note however, what may happen if the infected cell is not killed by the virus. The presence of the virus and the viral growth-promoting protein can drive the host cell into unceasing growth and cell division. This converts the host cell growth from a normal pattern to a pattern typical of cancer cells. The gene that encodes the growth-promoting protein can function as an oncogene that acts to transform the infected cell into a cancer cell
More than 90% of human cervical carcinomas are associated with infection by human papilloma virus a dsDNA virus that infects the lining of the cervix. In order for HPV to create a tumor the viral genome must perpetuate itself so when the original infected cell divides into many cells each new cell contains the virus and the viral growth promoting protein
The Epstein Barr dsDNA virus that results in mononucleosis in this country. For reasons that are unclear the Epstein Barr virus triggers Burkitts lymphoma in central Africa and a tumor of the nasal cavity in Southeast Asia. These tumors are inadvertent by products of the need to replicate viral DNA. The outgrowth of tumors happens on occasion when virus infected cells are not eliminated by the completion of the viral lytic cycle