how do viruses increase their number
Answers
Answer:
A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism.[1] Viruses infect all life forms, from animals and plants to microorganisms, including bacteria and archaea.[2][3] Since Dmitri Ivanovsky's 1892 article describing a non-bacterial pathogen infecting tobacco plants and the discovery of the tobacco mosaic virus by Martinus Beijerinck in 1898,[4] more than 9,000 virus species have been described in detail[5] of the millions of types of viruses in the environment.[6] Viruses are found in almost every ecosystem on Earth and are the most numerous type of biological entity.[7][8] The study of viruses is known as virology, a subspeciality of microbiology.
Answer:
The dynamics of viral infections have been studied extensively in a variety of settings, both experimentally and with mathematical models. The majority of mathematical models assumes that only one virus can infect a given cell at a time. It is, however, clear that especially in the context of high viral load, cells can become infected with multiple copies of a virus, a process called coinfection. This has been best demonstrated experimentally for human immunodeficiency virus (HIV), although it is thought to be equally relevant for a number of other viral infections. In a previously explored mathematical model, the viral output from an infected cell does not depend on the number of viruses that reside in the cell, i.e. viral replication is limited by cellular rather than viral factors. In this case, basic virus dynamics properties are not altered by coinfection.
Results
Here, we explore the alternative assumption that multiply infected cells are characterized by an increased burst size and find that this can fundamentally alter model predictions. Under this scenario, establishment of infection may not be solely determined by the basic reproductive ratio of the virus, but can depend on the initial virus load. Upon infection, the virus population need not follow straight exponential growth. Instead, the exponential rate of growth can increase over time as virus load becomes larger. Moreover, the model suggests that the ability of anti-viral drugs to suppress the virus population can depend on the virus load upon initiation of therapy. This is because more coinfected cells, which produce more virus, are present at higher virus loads. Hence, the degree of drug resistance is not only determined by the viral genotype, but also by the prevalence of coinfected cells.
Conclusions
Our work shows how an increased burst size in multiply infected cells can alter basic infection dynamics. This forms the basis for future experimental testing of model assumptions and predictions that can distinguish between the different scenarios.
Reviewers
This article was reviewed by RJdeB, RMR and MK.
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