Virus latency in the context of "Varicella zoster virus"

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⭐ Core Definition: Virus latency

Virus latency (or viral latency) is the ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the lysogenic part of the viral life cycle. A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which, after initial infection, proliferation of virus particles ceases. However, the viral genome is not eradicated. The virus can reactivate and begin producing large amounts of viral progeny (the lytic part of the viral life cycle) without the host becoming reinfected by new outside virus, and stays within the host indefinitely.

Virus latency is not to be confused with clinical latency during the incubation period when a virus is not dormant.

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👉 Virus latency in the context of Varicella zoster virus

Varicella zoster virus (VZV), also known as human herpesvirus 3 (HHV-3, HHV3), is one of nine known herpes viruses that can infect humans. It causes chickenpox (varicella), commonly affecting children and young adults, and shingles (herpes zoster) in adults but rarely in children. As a late complication of VZV infection, Ramsay Hunt syndrome type 2 may develop in rare cases. VZV infections are species-specific to humans. The virus can survive in external environments for a few hours.

VZV multiplies in the tonsils, and causes a wide variety of symptoms. Similar to the herpes simplex viruses, after primary infection with VZV (chickenpox), the virus lies dormant in neurons, including the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Many years after the person has recovered from initial chickenpox infection, VZV can reactivate to cause shingles.

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Virus latency in the context of Herpesviridae

Orthoherpesviridae, previously named and more widely known as Herpesviridae, is a large family of DNA viruses that cause infections and certain diseases in animals, including humans. The members of this family are commonly known as herpesviruses. The family name is derived from the Greek word ἕρπειν (herpein 'to creep'), referring to spreading cutaneous lesions, usually involving blisters, seen in flares of herpes simplex 1, herpes simplex 2 and herpes zoster (shingles). In 1971, the International Committee on the Taxonomy of Viruses (ICTV) established Herpesvirus as a genus with 23 viruses among four groups. Since then, the number of identified herpesviruses has grown to more than 100. Herpesviruses can cause both latent and lytic infections.

Nine herpesvirus types are known to primarily infect humans, at least five of which are extremely widespread among most human populations, and which cause common diseases: herpes simplex 1 and 2 (HSV-1 and HSV-2, also known as HHV-1 and HHV-2; both of which can cause orolabial and genital herpes), varicella zoster (VZV or HHV-3; the cause of chickenpox and shingles), Epstein–Barr (EBV or HHV-4; implicated in several diseases, including mononucleosis and some cancers), and human cytomegalovirus (HCMV or HHV-5). More than 90% of adults have been infected with at least one of these, and a latent form of the virus remains in almost all humans who have been infected. Other human herpesviruses are human herpesvirus 6A and 6B (HHV-6A and HHV-6B) and human herpesvirus 7 (HHV-7), which are the etiological agents for Roseola, and HHV-8 (also known as KSHV) which is responsible for causing Kaposi's sarcoma. HHV here stands for "Human Herpesvirus".

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Virus latency in the context of Shingles

Shingles, also known as herpes zoster or zona, is a viral disease characterized by a painful skin rash with blisters in a localized area. Typically the rash occurs in a single, wide mark either on the left or right side of the body or face. Two to four days before the rash occurs, there may be tingling or local pain in the area. Other common symptoms are fever, headache, and tiredness. The rash usually heals within two to four weeks, but some people develop ongoing nerve pain which can last for months or years, a condition called postherpetic neuralgia (PHN). In those with poor immune function the rash may occur widely. If the rash involves the eye, vision loss may occur.

Shingles is caused by the varicella zoster virus (VZV) that also causes chickenpox. In the case of chickenpox, also called varicella, the initial infection with the virus typically occurs during childhood or adolescence. Once the chickenpox has resolved, the virus can remain dormant (inactive) in human nerve cells (dorsal root ganglia or cranial nerves) for years or decades, after which it may reactivate and travel along nerve bodies to nerve endings in the skin, producing blisters. During an outbreak of shingles, exposure to the varicella virus found in shingles blisters can cause chickenpox in someone who has not yet had chickenpox, although that person will not suffer from shingles, at least on the first infection. How the virus remains dormant in nerve cells or subsequently re-activates is not well understood.

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Virus latency in the context of Lysogeny

Lysogeny, or the lysogenic cycle, is one of two cycles of viral reproduction (the lytic cycle being the other). Lysogeny is characterized by integration of the bacteriophage nucleic acid into the host bacterium's genome or formation of a circular replicon in the bacterial cytoplasm. In this condition the bacterium continues to live and reproduce normally, while the bacteriophage lies in a dormant state in the host cell. The genetic material of the bacteriophage, called a prophage, can be transmitted to daughter cells at each subsequent cell division, and later events (such as UV radiation or the presence of certain chemicals) can release it, causing proliferation of new phages via the lytic cycle.

Lysogenic cycles can also occur in eukaryotes, although the method of DNA incorporation is not fully understood. For instance, the HIV viruses can either infect humans lytically, or lay dormant (lysogenic) as part of the infected cells' genome, keeping the ability to return to lysis at a later time.

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