What is the difference between latent and persistent viral infections

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Recommend AccessScience to your librarian. One viral protein blocks translocation of peptides into the lumen of the endoplasmic reticulum, while two other viral proteins cause degradation of MHC class I proteins before they reach the cell surface. There are many more examples of how virus infections modulate the immune response, leading to persistent infection. Not surprisingly, many of the processing or regulatory steps that are targets of viral modulation were not even known until it was discovered that they were blocked by virus infection.

Peterhans, E. Bornkamm, G. Although the mechanisms by which viruses produce persistent infection are not completely understood, some common factors have been identified. The first is immune modulation. Many viruses that cause persistent infection avoid the specific and nonspecific immune defenses in several ways.

Examples include:. Limitation of recognition molecules on infected cells: a. Restricted expression of viral antigens e. Antiviral antibody-induced internalization and modulation of viral antigens e. Decreased expression of cell major histocompatibility complex recognition molecules e. Altered lymphocyte and macrophage functions, including modified production of cytokines and immunosuppression e.

Infection in immunologically privileged anatomic sites e. Since the viruses multiple at a rapid rate, by the end of the latent period billions of viral particles are produced.

In this situation the virus exists in an occult noninfectious form. Figure Hepatitis B Viral Antigen and Antibody levels detected in the blood after an acute infection.

Following viruses and viral infections can be taken as examples of latent viral infections. Clinical features of an infection appear during this stage of the infection. The persistence of viral infection is partially contributed by the virus not interrupting the vital metabolic processes of the host cells.

Infection of thymic epithelial cells with LCMV induces tolerance of new T cells derived from bone marrow progenitors. Viral latency is characterized by decreased viral gene expression and is another mechanism by which viruses avoid immune surveillance and establish persistent infections. Upon the initial infection of host cells, they commence production of new viral progeny, which results in the death of the infected cells. This is referred to as the lytic cycle of the virus.

Viruses derived from the primary site of infection either can produce more viral progeny upon infection of additional cells or can establish a latent infection during which viral protein production is virtually shut off T cells can recognize herpesvirus antigens during the lytic cycle of the virus but fail to detect a target during latency.

Different types of herpesvirus differ in their tropism and hence in their pathogenicity. Herpes simplex viruses initially infect epithelial cells and then, upon retrograde axonal transport, establish latent infections in neurons. Upon reactivation, the virus is transported back to the skin or mucosa, where it replicates It can cause lymphoproliferative disease and lymphomas in immunosuppressed individuals This can be treated in transplant recipients by lowering of the immunosuppressive regimen, which allows resurgence of T cells that eliminate the EBV-infected B cells.

Patients with X-linked hyperproliferative disease are prone to develop fulminant infections with EBV Cytomegalovirus persists in cells of the bone marrow, and, again, immunosuppressed individuals are at increased risk for fatal infections after viral reactivation Most HPVs cause harmless, albeit unattractive, proliferation of keratinocytes in the skin or the genital mucosa. Skin warts, which are common in children, often regress spontaneously, presumably upon activation of an immune response.