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Index >>Viruses and Cancer >>Polyoma and SV40 Viruses

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Viruses and Cancer Types of Cancer Characteristics of Cancer Cells Somatic Mutation Hypothesis Viral Gene Hypothesis Defective Immunity Hypothesis Other Theories for Viral and Chemical Carcinogensis DNA Viruses RNA Viruses Incorporation of Viral DNA in to the Genome of the Host List of Chemical Carcinogens Oncogenic Viruses - Papovaviruses

Polyoma and SV40 Viruses

	Polyoma and SV40 Viruses - Both these viruses are similar in size and general structure. The viral particles are about 45 nm in diameter. The capsid is icosahedral and consists of 72 capsomers, with the triangulation number T=7. The MW of DNA is 3-3.5 x 10 power 6 daltons. It contain about 5,000 nucleotide pairs. In both viruses the native form (Form I) of DNA is the super coiled, covalently closed circular double helix, with a sedimentation coefficient of 218. A single strand break by cleavage of phosphodiester bond converts the super coiled DNA into a relaxed circular form (Form II) with a sedimentation coefficient of 16S.
A double stranded break of the super coiled form converts it into the linear form (form III) with a sedimentation coefficient of l4S. In the polyoma virus the G+C content is 47-50 per cent, while in SV40 it is 41 per cent. The polyoma virus is responsible for tumours in mice, The virus can be cultured in permissive mouse cell lines, the cells of support replication and growth of the virus. The virus undergoes lytic cycle in which the host cells ultimately die and liberate a large number of virus particles The virus can also infect rat and hamster cells, which are transformed into tumour cells without liberating large amounts of virus particles. Such infection is said to be non lytic, and the cells are called non permissive cells.
Proteins : The proteins may be considered under two heads, early proteins and late proteins early proteins. Early after infection before the replication of DNA begins, the T antigen (or tumour - antigen) can be detected in the cell nucleus. The synthesis of the T antigen is inhibited by interferon, which specifically inhibits viral protein synthesis but not cell protein synthesis. This suggests that the T antigen is coded by the virus DNA. More direct evidence for this comes from microinjection experiments in which SV40 RNA complementary to early viral DNA was injected into epithelial cells in a mouse cell culture.
The T antigen was found in the cells after 4-5 hours. After the appearance of the T antigen several DNA metabolism enzymes begin to increase in concentration in infected cells. These include DNA polymerase, DNA ligase and thymidine kinase. They appear to be coded by the host cell, as the viral genome is insufficient for coding them. Late proteins : The capsid (structural) proteins are the late proteins. In SV 40 only two capsid proteins have been identified. These are the major capsid protein VPI (MW 45,000) and the minor capsid protein VP2 (MW 30,000). VP5 may be present, but the data are not consistent. The polyoma viruses have the capsid proteins VP, VP2 and V 3. There are common sequences in VP2 and VP3, but no common sequences between the major capsid protein VP1 and the minor capsid proteins VP2/VP3

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List of Some Papovaviruses Polyoma and SV 40 Viruses Replication of DNA Protein Synthesis Retroviruses Proteins of the Murine Leukemia Virus Oncornavirus Replicative Cycle Types of Tumor Virus Infection Abortive Infection Defective Infection Nonpermissive Infection Inactive Infection Defective and Helper Viruses Transmission of Oncornaviruses

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