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Viral Genome Integration into the Host Cell Genome: A Double Edged-Sword #MMPMID35221000
da Mata Kanzaki ECG; Kanzaki I
Discov Med 2021[Nov]; 32 (167): 141-148 PMID35221000show ga
Genetic information exchange between virus and host cells apparently seems to be detrimental, as pluricellular organisms could develop diseases. Nevertheless, during billion years long evolutionary processes, the cell's genome revealed a mosaic of viral genomes or gene segments, giving rise to speculations that the genome of any cell was constructed and shaped by the invasion of virus genomes. But it could also be interpreted that the cellular genome is the source of autonomous gene segments that escaped from the cells, at some conditions, as a threat to the cell's survival. Quite commonly, oncogenic viruses integrate their genome in the host cell genome or interact in their episomal form. Some of these viruses cause lytic infection alternated with latent and persistent infection, leading to chronic inflammation, ultimately resulting in autoimmune diseases and cancer. Rarely, but potentially occurring, the genome of non-oncogenic RNA viruses could gain access to the cell nucleus, and eventually integrate their gene segments or genome in the host chromosome as it has been postulated for the current agent of the Corona Virus Disease 2019 (COVID-19), the Severe Acute Respiratory Syndrome Coronavirus type 2 (SARS-CoV-2). Rather than re-infection, SARS-CoV-2 gene activation, from host chromosome integrated material, would explain the detection of virus gene segments as in viremia. Therefore, viral capsids or solely viral gene segments, actively and selectively transported to the cell nucleus, could be found taking into account the exuberant virome reaching the cell nucleus to perform their replicative cycle. So, would the integration of unconventional reverse transcribed viral RNA of SARS-CoV-2, and of other RNA viruses, as the Bornaviruses, lead to the production of transcripts and proteins inducing antigenemia and stimulating constant immune response, or else would result in the excessive activation of neighboring cellular genes with pathogenic role to the host cell?