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Herpesviruses (Human)

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Abstract Human herpesviruses are a family of eight deoxyribonucleic acid (DNA) viruses. There are three subfamilies, reflecting size and sites of latency. The alphaherpesviruses consist of Herpes simplex virus type 1 (HSV‐1), Herpes simplex virus type 2 (HSV‐2) and Varicella‐zoster virus (VZV), all of which have a predisposition to infect neuronal tissues and establish latency in sensory ganglia. The betaherpesviruses are Cytomegalovirus (CMV), Human herpesvirus 6 (HHV‐6) and Human herpesvirus 7 (HHV‐7) which infect endothelial cells and secretory glands. Finally, the gamma herpesviruses are Epstein – Barr virus (EBV) and Kaposi sarcoma‐associated herpesvirus (KSHV or HHV‐8). These viruses commonly infect humans but generally cause only trivial disease. However, in high‐risk patient populations (e.g. the newborn or immunocompromised host) disease can be associated with significant morbidity and mortality. Therapy exists for many but not all of the resultant diseases. Key Concepts: Human herpesviruses are a family of eight deoxyribonucleic acid (DNA) viruses: Herpes simplex virus type 1 (HSV‐1), Herpes simplex virus type 2 (HSV‐2), Varicella‐zoster virus (VZV), Cytomegalovirus (CMV), Epstein‐Barr virus (EBV), Human herpesvirus 6 (HHV‐6), Human herpesvirus 7 (HHV‐7) and Kaposi sarcoma‐associated herpesvirus (KSHV or HHV‐8). Membership in the Herpesviridae family is based on the structure of the virion, and herpesvirus is categorised into three subfamilies and six groups (classified A–F) based on genomic sequence arrangement. Replication of herpesviruses occurs in a multistep process, though this process is considered inefficient, with a high ratio of noninfectious to infectious viral particles. Latency is established in specific host cells, and the latent viral genome may be either extrachromosomal or integrated into host cell DNA. Reactivation of latent virus can be triggered by such stimuli as stress, menstruation and exposure to ultraviolet light, though reactivation in not clearly understood from a biochemical of genetic standpoint. The definitive diagnosis of a herpesvirus infection usually requires either isolation of virus or the amplification of viral DNA by molecular techniques, namely polymerase chain reaction (PCR). A critical factor for the transmission of HSV‐1 and HSV‐2 is the requirement for intimate contact between a person who is shedding virus and a susceptible host. Varicella‐zoster virus is one of the most common encountered by humans, and is generally transmitted via airborne routes. Varicella (chicken pox) is the manifestation of primary infection, and Herpes zoster (shingles) is the recurrent form, resulting from latent virus. Vaccines are available for the prevention of both these types of infection. Infections due to HSV, VZV and CMV are the most amenable to therapy with antiviral drugs.
Title: Herpesviruses (Human)
Description:
Abstract Human herpesviruses are a family of eight deoxyribonucleic acid (DNA) viruses.
There are three subfamilies, reflecting size and sites of latency.
The alphaherpesviruses consist of Herpes simplex virus type 1 (HSV‐1), Herpes simplex virus type 2 (HSV‐2) and Varicella‐zoster virus (VZV), all of which have a predisposition to infect neuronal tissues and establish latency in sensory ganglia.
The betaherpesviruses are Cytomegalovirus (CMV), Human herpesvirus 6 (HHV‐6) and Human herpesvirus 7 (HHV‐7) which infect endothelial cells and secretory glands.
Finally, the gamma herpesviruses are Epstein – Barr virus (EBV) and Kaposi sarcoma‐associated herpesvirus (KSHV or HHV‐8).
These viruses commonly infect humans but generally cause only trivial disease.
However, in high‐risk patient populations (e.
g.
the newborn or immunocompromised host) disease can be associated with significant morbidity and mortality.
Therapy exists for many but not all of the resultant diseases.
Key Concepts: Human herpesviruses are a family of eight deoxyribonucleic acid (DNA) viruses: Herpes simplex virus type 1 (HSV‐1), Herpes simplex virus type 2 (HSV‐2), Varicella‐zoster virus (VZV), Cytomegalovirus (CMV), Epstein‐Barr virus (EBV), Human herpesvirus 6 (HHV‐6), Human herpesvirus 7 (HHV‐7) and Kaposi sarcoma‐associated herpesvirus (KSHV or HHV‐8).
Membership in the Herpesviridae family is based on the structure of the virion, and herpesvirus is categorised into three subfamilies and six groups (classified A–F) based on genomic sequence arrangement.
Replication of herpesviruses occurs in a multistep process, though this process is considered inefficient, with a high ratio of noninfectious to infectious viral particles.
Latency is established in specific host cells, and the latent viral genome may be either extrachromosomal or integrated into host cell DNA.
Reactivation of latent virus can be triggered by such stimuli as stress, menstruation and exposure to ultraviolet light, though reactivation in not clearly understood from a biochemical of genetic standpoint.
The definitive diagnosis of a herpesvirus infection usually requires either isolation of virus or the amplification of viral DNA by molecular techniques, namely polymerase chain reaction (PCR).
A critical factor for the transmission of HSV‐1 and HSV‐2 is the requirement for intimate contact between a person who is shedding virus and a susceptible host.
Varicella‐zoster virus is one of the most common encountered by humans, and is generally transmitted via airborne routes.
Varicella (chicken pox) is the manifestation of primary infection, and Herpes zoster (shingles) is the recurrent form, resulting from latent virus.
Vaccines are available for the prevention of both these types of infection.
Infections due to HSV, VZV and CMV are the most amenable to therapy with antiviral drugs.

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