Retrovirus has a unique machinery for its replication in
the host cells. Most RNA viruses, either ssRNA viruses or dsRNA viruses,
replicate their own genetic material and translate to viral proteins to activate
numerous biological functions. There is no DNA generated in their life cycles.
Distinct from other RNA viruses, however, retrovirus uses its own RNA-dependent
reverse transcriptase to synthesis viral DNA, and then integrate to cellular
genome to fulfill the central dogma.
The strategy of retroviral reverse transcription and
integration leads to the oncology of retrovirus. There are many oncogenes
presented in the host genome, which remains silence (with no transcription and
translation of the protein) until viral promoters are integrated in a certain
position of the genome, resulting the transcription of the oncogenes. With
accordance of Astrin et al, avian leukemia virus (ALV) is proved to have the
capability to insert its viral promoters to the cellular genome and activate
c-onc (cellular oncogene). This special trait is the major cause of neoplastic
formation of ALV (Hayward,
1981).
Nevertheless, as for the majority of retroviral
infection, the formation of oncology is not efficient as expected, since the
integration of viral promoters will be trade off with the integration and
replication of other essential genes of the virus, including gag, pol and env.
The virus loses its basic element to try so hard to activate cellular
oncogenes. The failure indicates that most retrovirus causes cancer with the
evasion of another helper viruses, like the co-infection of hepatitis B virus
(HBV) and hepatitis C virus (HCV). Helper virus is necessary for most
retroviral oncology, but not for Rous sarcoma virus (RSV). It has an
outstanding mechanism to simultaneously maintain the oncology and its efficient
replication.
References
Hayward, W.
S. (1981). Activation of a cellular onc gene by promoter insertion in
ALV-induced lymphoid leukosis. Nature, 290(5806), 475.
doi:10.1038/290475a0
The
following figure illustrates how ALV integrates its own promoter to the
cellular genome, as a very old but groundbreaking finding in 1981, Nature
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