I've heard in many talks as a passing, well-known fact that viruses(e.g. pathogenic HPV strains) offer selective advantage for the infected cell to multiply. But I'm not able to quite wrap my head around this.

I assume this has something do with episomal qualities of viruses, but how exactly does that does translate to selective advantage.

My intuition says that if there is an uneven segregation of the viral genomes to the daughter cells, than that heterogeneity can cause give selective advantage. But given no preface of the heterogeneity of a virus during cell division, how is one able to claim that viruses offer selective advantage?

Background: I am not a biology person, but rather computational scientist who works with biologists. one example source


See the instances of "selective advantage / pressure" from the source provided by Jonathan, emphasis mine:

Persistent infection with HPV leads to an environment of genomic instability and local immune suppression, which can lead to both the accumulation of genomic alterations in the host cell, as well as to the integration of the viral genome into the host genome. When these additional alterations provide a selective growth advantage to the cell, carcinogenesis may ensue.

Furthermore, the integrated viral transcripts confer stronger transforming capacity than those derived from episomes, due to longer half-life of transcripts (32). This promotes immortalization and transformation of these cells and provides a selective growth advantage (3, 8, 30, 33). Integration may, however, confer a selective growth advantage to the host cells not only through its effects on the viral genome (i.e., enhanced/deregulated expression of viral oncoproteins), but also through its effects on the host genome (i.e., by affecting key cellular genes).

Several mechanisms by which HPV integration may confer a selective advantage have been described (Fig. 3).

This environment is also amenable to accumulation of genetic alterations and viral integration, and subsequent tumor formation. Integration affects both the viral genome and the host genome, likely conferring additional neoplastic selective pressure, by one or more of the following mechanisms: (i) enhanced expression of viral oncoproteins, (ii) alteration of critical cellular genes (leading to increased expression of oncogenic proteins, decreased expression of tumor suppressor proteins, altered DNA repair mechanisms, or modulation of the immune system), and (iii) changes in global promoter methylation and transcription.

In biology, "selection" often refers to natural selection -- in short, genetic diversity in a population manifests as different traits in individuals, which result in differences in relative fitness in a given environment that, through time, result in evolution. The quoted excerpts refer not to the environment acting on different traits but rather to the (potential) enhanced growth characteristics of HPV-infected cells, relative to non-infected cells. So, the use of "selective" here is misleading. Yes, viral integration may lead to enhanced growth of a cell population by disruption of certain cell cycle checkpoint genes, but the organism on the whole will certainly be less fit when that unrestricted growth leads to cancer.

In my opinion, the text could read "growth advantage" or "enhanced growth" in all instances and do away with "selective" entirely.

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    $\begingroup$ I believe they use the term "selective" in reference to experiments where infected and non-infected cells are co-cultured. Over time, infected cells become a larger fraction of the population due to increased replication/survival of those cells, so they can say that in the culture environment (where cells are acting more like individual single-cell organisms than like members of a multicellular animal) there is a selective advantage to being infected with HPV. I agree with you, though, that the word is not particularly important and could be omitted. $\endgroup$ – Bryan Krause Nov 9 '20 at 18:42

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