Human herpesvirus six: Difference between revisions
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==Treatment== | |||
===Antimicrobial Regimen=== | |||
:* '''Human herpesvirus 6 treatment'''<ref name="pmid25582535">{{cite journal| author=Tong LX, Worswick SD| title=Viral infections in acute graft-versus-host disease: a review of diagnostic and therapeutic approaches. | journal=J Am Acad Dermatol | year= 2015 | volume= 72 | issue= 4 | pages= 696-702 | pmid=25582535 | doi=10.1016/j.jaad.2014.12.002 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25582535 }} </ref><ref name="pmid15653828">{{cite journal| author=De Bolle L, Naesens L, De Clercq E| title=Update on human herpesvirus 6 biology, clinical features, and therapy. | journal=Clin Microbiol Rev | year= 2005 | volume= 18 | issue= 1 | pages= 217-45 | pmid=15653828 | doi=10.1128/CMR.18.1.217-245.2005 | pmc=PMC544175 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15653828 }} </ref> | |||
::* Preferred regimen: supportive therapy | |||
::* Note: If patient is immunocompromised, there are no antiviral regimens stablished as there are no clinical trials to validate their use on these cases. Consider administering [[Ganciclovir]], [[Acyclovir]], [[Foscarnet]] {{or}} [[Cidofovir]].<ref name="pmid22819486">{{cite journal| author=Wolz MM, Sciallis GF, Pittelkow MR| title=Human herpesviruses 6, 7, and 8 from a dermatologic perspective. | journal=Mayo Clin Proc | year= 2012 | volume= 87 | issue= 10 | pages= 1004-14 | pmid=22819486 | doi=10.1016/j.mayocp.2012.04.010 | pmc=PMC3538396 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22819486 }} </ref><ref name="pmid15653828">{{cite journal| author=De Bolle L, Naesens L, De Clercq E| title=Update on human herpesvirus 6 biology, clinical features, and therapy. | journal=Clin Microbiol Rev | year= 2005 | volume= 18 | issue= 1 | pages= 217-45 | pmid=15653828 | doi=10.1128/CMR.18.1.217-245.2005 | pmc=PMC544175 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15653828 }} </ref> | |||
==References== | ==References== | ||
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[[fr:Herpèsvirus humain type 6]] | [[fr:Herpèsvirus humain type 6]] | ||
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Latest revision as of 19:27, 7 August 2015
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 Electron micrograph of HHV-6
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Human herpesvirus 6 (HHV-6) |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Human Herpesvirus Six (HHV-6) is one of the eight known viruses that are members of the human herpesvirus family.
Groupings
HHV-6 is a member of the betaherpesviridae (subfamily of the herpesvirinae) which also includes HHV-7 and Cytomegalovirus (HHV-5 or HCMV). There are two subtypes of HHV-6 termed HHV-6A and HHV-6B.
Occurrence
HHV-6B is responsible for up to 93% of primary infections in Europe and North America. Such infections usually cause fever, with exanthem subitum (Roseola/rash)[1] only being observed in 10% of cases. HHV-6 primary infections account for up to 20% of infant hospitalizations in the United States and are associated with several more severe complications, such as encephalitis, lymphadenopathy, myocarditis and myelosuppression.
After primary infection, latency is established in myeloid and bone marrow progenitors and exists for the life time of the host. The virus periodically re-activates from this latent state, with HHV-6 DNA being detectable in 20-25% of healthy adults in the United States. In the immunocompetent setting, these re-activations are often asymptomatic, but in immunosuppressed, individuals there can be serious complications.
HHV-6 re-activation causes severe disease in transplant recipients and can lead to graft rejection, often in consort with other betaherpesviridae. Likewise in HIV/AIDS, HHV-6 re-activations cause disseminated infections leading to end organ disease and death. Although up to 100% of the population are exposed (seropositive) to HHV-6, most by 3 years of age, there are rare cases of primary infections in adults. In the United States, these have been linked more with HHV-6A, which is thought to be more pathogenic and more neurotropic and has been linked to several central nervous system-related disorders.
HHV-6 has also been found in multiple sclerosis patients[2] and has been implicated as a co-factor in several other diseases, including chronic fatigue syndrome[3], fibromyalgia, AIDS[4], and temporal lobe epilepsy[5] but no definitive link has been established.
Treatment
Antimicrobial Regimen
References
- ↑ Newly Found Herpes Virus Is Called Major Cause of Illness in Young, New York Times
- ↑ Prevalence of herpesvirus DNA in MS patients, Acta Neurol Scand
- ↑ CFS: Evaluation and Treatment, Amer Academy of Family Physicians
- ↑ HHV-6 and AIDS, Wisconsin Viral Research Group
- ↑ Fotheringham J, Donati D, Akhyani N, Fogdell-Hahn A, Vortmeyer A, Heiss JD, Williams E, Weinstein S, Bruce DA, Gaillard WD, Sato S, Theodore WH, Jacobson S (2007). "Association of human herpesvirus-6B with mesial temporal lobe epilepsy". PLoS Med. 4 (5): e180. doi:10.1371/journal.pmed.0040180. PMID 17535102.
- ↑ Tong LX, Worswick SD (2015). "Viral infections in acute graft-versus-host disease: a review of diagnostic and therapeutic approaches". J Am Acad Dermatol. 72 (4): 696–702. doi:10.1016/j.jaad.2014.12.002. PMID 25582535.
- ↑ 7.0 7.1 De Bolle L, Naesens L, De Clercq E (2005). "Update on human herpesvirus 6 biology, clinical features, and therapy". Clin Microbiol Rev. 18 (1): 217–45. doi:10.1128/CMR.18.1.217-245.2005. PMC 544175. PMID 15653828.
- ↑ Wolz MM, Sciallis GF, Pittelkow MR (2012). "Human herpesviruses 6, 7, and 8 from a dermatologic perspective". Mayo Clin Proc. 87 (10): 1004–14. doi:10.1016/j.mayocp.2012.04.010. PMC 3538396. PMID 22819486.
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