Viral Infection Process

Steps of Viral Infections

Virus infection stages can approximately divide into five stages. The virus replication may be blocked at any point from virus attachment to the final stages of virion release. The stages of virus infection are described as follows.

  • Attachment. Viruses attach to the cell surface and bind to its receptors via glycoproteins or other proteins on the surface of viruses.
  • Penetration. Viruses can fuse with the membrane to release viral internal components into the cell. Viruses also can hijack the clathrin-mediated endocytosis, caveolin-mediated endocytosis, non-clathrin, and non-caveolin endocytosis to enter the cell.
  • Replication. The virus takes advantage of the host cell structures to produce virus components and replicate itself. The virus can fuse with the late endosomes to release the capsid or genome, and the capsids can also be transported by kinesin to release the genome into the replication site of the nucleus.
  • Assembly.
    • Nonenveloped viruses exhibit full maturation in the cytoplasm (e.g., picornaviruses) or the nucleus (e.g., adenoviruses) with disintegration of the cell and release of virions.
    • Enveloped viruses. When virus protein and nucleic acid components have been replicated, the viral genome is transported to the microtubule organizing center (MTOC) and packaged into the capsid. The capsid can be transported to the cell periphery, then assemble and bud. The capsid also can be enveloped in the multi-vesicular body (MVB) or Golgi to form the complete virus.
  • Release.
    • Budding release. The virus can be transported to the cytoplasmic membrane to bud and exit the cell.
    • Lysis release. Some infected cells die through cell lysis or apoptosis to release all virions.

Then the released viruses can carry out a new cycle of infection again.

Viral infection process in live cells Fig1 Viral infection process in live cells. (Liu, 2016)

Types of Viral Infections

Classification according to the disease progression caused by viral infection.

  • Acute infections. Acute viral infection is a nonequilibrium process. The characteristic of acute infection is the short latent period and acute onset, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
  • Persistent Infection. Persistent infection involves a delicate balance between virus and host that may allow the survival of viruses in the host. Then viruses may be reactivated and cause recrudescent episodes of disease, or they may cause immunopathologic disease or neoplasia. This result of persistent infection may be due to weak antigenicity, immune escape, and the integration of viral genes into the host cell. Viruses such as Hepatitis B virus (HBV) and human immunodeficiency virus (HIV), that cause persistent infections, can be shed at lower titers for months to years but will eventually be transmitted during the course of a long-lasting infection. The immunologic approach may not be effective in eliminating or controlling a given persistent infection. The course of the infection can take one of three ways:chronic infections, latent infections, and slow viral infections.
    • Chronic infections. After clinical or subclinical infection, the virus continues to multiply very slowly but continuously. Some viruses can integrate their genome into the cell, some not. Chronic viral infections cause persistent infections which may last for months or years.
    • Latent infections. The virus remains in an asymptomatic host cell for long periods. Latency maintains the viral genome for the lifetime of the infected host without activation. Though the virus remains most of the time hidden without replication, it can reactivate resulting in clinical manifestations.
    • Slow infections, in which quantities of the infectious virus gradually increase during a very long preclinical phase that eventually leads to slowly progressive disease. This kind of infection has a long incubation period that lasts for months or years, symptoms usually do not occur during the incubation period.

The Course of Viral Infection: Comparing Acute and Chronic Viral Infection. Fig2 The Course of Viral Infection: Comparing Acute and Chronic Viral Infection. (Virgin, 2009)

Major Infection Mechanisms

Cytopathic viruses kill the cells in which they replicate, by preventing the synthesis of host macromolecules, by producing degradative enzymes or toxic products, or by inducing apoptosis. The mechanisms include:

  • Inhibition of host-cell nucleic acid synthesis, RNA transcription, processing of host-cell messenger RNAs, and protein synthesis.
  • Cytopathic effects of “toxic”.
  • Interference with cellular membrane function viral proteins.

Some viruses usually do not kill the cells in which they replicate, such as a few kinds of RNA viruses, retroviruses, and some paramyxoviruses. They usually lead to persistent infection and release of virions but overall cellular metabolism is little affected.

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  1. Liu SL; et al. Tracking single viruses infecting their host cells using quantum dots. Chem Soc Rev, 2016. 45(5): 1211-1224.
  2. Virgin H.W; et al. Redefining chronic viral infection. Cell, 2009. 138(1): 30-50.

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