Viruses multiply only in living cells. The host cell provides the energy and synthetic machinery and the low-molecular-weight precursors for the synthesis of viral proteins and nucleic acids. The viral nucleic acid carries the genetic specificity to code for all of the virus-specific macromolecules in a highly organized fashion.

For a virus to replicate, viral proteins must be synthesized by the host cell protein-synthesizing machinery. There fore, the virus genome must be able to produce a functional mRNA. Various mechanisms have been identified that allow viral RNAs to compete successfully with cellular mRNAs to produce adequate amounts of viral proteins.

 The unique feature of viral multiplication is that soon after interaction with a host cell the infecting virion is disrupted and its measurable infectivity is lost. This phase of the growth cycle is called the eclipse period; its duration varies depending on both the particular virus and the host cell, and it is followed by an interval of rapid accumulation of infectious progeny virus particles. The eclipse period is actually one of intense synthetic activity as the cell is redirected toward fulfilling the needs of the viral parasite. In some cases, as soon as the viral nucleic acid enters the host cell, the cellular  metabolism is redirected exclusively toward the synthesis of new virus particles and the cell is destroyed. In other cases, the metabolic processes of the host cell are not altered significantly, although the cell synthesizes viral proteins and nucleic acids, and the cell is not killed.

 After the synthesis of viral nucleic acid and viral proteins , the components assemble to form new infectious virions. The yield of infectious virus per cell ranges widely, from modest numbers to more than 100,000 particles. The duration of the virus replication cycle also varies widely, from 6 to 8 hours (picornaviruses) to more than 40 hours (some herpesviruses).

Not all infections lead to new progeny virus. Productive infections occur in permissive cells and result in the production  of infectious virus. Abortive infections fail to produce infectious progeny, either because the cell may be nonpermissive and unable to support the expression of all viral genes or because the infecting virus may be defective, lacking  some functional viral gene. A latent infection may ensue, with the persistence of viral genomes, the expression of no or a few viral genes, and the survival of the infected cell. The pattern of replication may vary for a given virus, depending on the type of host cell infected

مواضيع ذات صلة

Adenovirus Coinfection with SARS-CoV-2

Genetic Polymorphisms susceptibility to SARS-CoV-2

Acute viral hepatitis

Human receptor of coronavirus and Adenovirus

Antiviral Chemotherapy

Humoral Immune Responses to SARS-CoV-2 Infection

Cellular Immune Responses to SARS-CoV-2

Pathogenesis of SARS-CoV-2

Epidemiology of SARS-CoV-2

PARVOVIRIDAE

تركيب فيروس التهاب الكبد الوبائي نوع ب الخفي

مرض الجدري Smallpox