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*In majority of [[immunocompetent]] people, primary [[Cytomegalovirus infection|CMV infection]] is sub clinical and asymptomatic. | *In majority of [[immunocompetent]] people, primary [[Cytomegalovirus infection|CMV infection]] is sub clinical and asymptomatic. | ||
*Following primary infection the [[virus]] persists in a latent form in the host tissues invading the [[immune system]]. | *Following primary infection the [[virus]] persists in a latent form in the host tissues invading the [[immune system]]. | ||
*Reactivation can occur in response to [[inflammatory]] stimuli, physiologic stress and immunosuppression releasing new virions that can infect new cells causing cmv end organ infection. | *Reactivation can occur in response to [[inflammatory]] stimuli, physiologic [[stress]] and [[immunosuppression]] releasing new [[virions]] that can infect new cells causing cmv end organ infection. | ||
*T-cells play a role in controlling the replication of the virus. | *[[T-cells]] play a role in controlling the [[replication]] of the [[virus]]. | ||
*In patients with T-cell deficiency the viral replication is uncontrolled and results in excessive shedding of the virus. | *In patients with [[T cell|T-cell]] deficiency the viral [[replication]] is uncontrolled and results in excessive shedding of the [[virus]]. | ||
*Reactivation of the virus results in the release of cytokines such as TNF-α and IFN-γ resulting in inflammation. | *Reactivation of the [[virus]] results in the release of [[cytokines]] such as [[TNF-α]] and [[Interferon gamma|IFN-γ]] resulting in [[inflammation]]. | ||
===Genetics=== | ===Genetics=== | ||
*Patients with polymorphisms in the genes coding for mannose binding lectin and ficolin-2 are at a higher risk of developing CMV infection.<ref name="pmid27108521">{{cite journal| author=Klenerman P, Oxenius A| title=T cell responses to cytomegalovirus. | journal=Nat Rev Immunol | year= 2016 | volume= 16 | issue= 6 | pages= 367-77 | pmid=27108521 | doi=10.1038/nri.2016.38 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27108521 }} </ref> | *Patients with [[polymorphisms]] in the [[genes]] coding for mannose binding [[lectin]] and ficolin-2 are at a higher risk of developing [[CMV infection]].<ref name="pmid27108521">{{cite journal| author=Klenerman P, Oxenius A| title=T cell responses to cytomegalovirus. | journal=Nat Rev Immunol | year= 2016 | volume= 16 | issue= 6 | pages= 367-77 | pmid=27108521 | doi=10.1038/nri.2016.38 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27108521 }} </ref> | ||
===Associated Conditions=== | ===Associated Conditions=== | ||
*Symptomatic cytomegalovirus is associated with HIV infection in majority of patients.<ref name="pmid27714898">{{cite journal| author=Grønborg HL, Jespersen S, Hønge BL, Jensen-Fangel S, Wejse C| title=Review of cytomegalovirus coinfection in HIV-infected individuals in Africa. | journal=Rev Med Virol | year= 2017 | volume= 27 | issue= 1 | pages= | pmid=27714898 | doi=10.1002/rmv.1907 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27714898 }} </ref><ref name="pmid27625433">{{cite journal| author=Gianella S, Letendre S| title=Cytomegalovirus and HIV: A Dangerous Pas de Deux. | journal=J Infect Dis | year= 2016 | volume= 214 Suppl 2 | issue= | pages= S67-74 | pmid=27625433 | doi=10.1093/infdis/jiw217 | pmc=5021239 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27625433 }} </ref> | *Symptomatic [[cytomegalovirus]] is associated with [[HIV AIDS|HIV infection]] in majority of patients.<ref name="pmid27714898">{{cite journal| author=Grønborg HL, Jespersen S, Hønge BL, Jensen-Fangel S, Wejse C| title=Review of cytomegalovirus coinfection in HIV-infected individuals in Africa. | journal=Rev Med Virol | year= 2017 | volume= 27 | issue= 1 | pages= | pmid=27714898 | doi=10.1002/rmv.1907 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27714898 }} </ref><ref name="pmid27625433">{{cite journal| author=Gianella S, Letendre S| title=Cytomegalovirus and HIV: A Dangerous Pas de Deux. | journal=J Infect Dis | year= 2016 | volume= 214 Suppl 2 | issue= | pages= S67-74 | pmid=27625433 | doi=10.1093/infdis/jiw217 | pmc=5021239 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27625433 }} </ref> | ||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
* | *[[CMV infection]] demonstrates the presence of [[intranuclear]] [[inclusion]] bodies. These [[inclusion bodies]] stain dark pink on an [[H&E stain]], and are also called "Owl's Eye" [[inclusion bodies]]. | ||
==References== | ==References== | ||
Revision as of 17:30, 30 May 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]
Overview
Transmission of CMV occurs from person to person and primary CMV infection causes activation of the immune system and resulting in a mononucleosis like presentation with hepatitis in immunocompromised individuals and few immunocompetent individuals. Reactivation can occur in response to inflammatory stimuli, physiologic stress and immunosuppression releasing new virions that can infect new cells causing CMV end organ infection.
Pathophysiology
Transmission
- Transmission of CMV occurs from person to person.
- Infection requires close, intimate contact with a person excreting the virus in their saliva, urine, blood, tears, and semen.
- The shedding of virus may take place intermittently, without any detectable signs, and without causing symptoms.
- CMV can be sexually transmitted and can also be transmitted via breast milk, transplanted organs, and rarely from blood transfusions.[1]
Pathogenesis
- Primary CMV infection causes activation of the immune system and results in a mononucleosis like presentation and its complications in immunocompromised individuals and few immunocompetent individuals.[2][3][4][5][6]
- In majority of immunocompetent people, primary CMV infection is sub clinical and asymptomatic.
- Following primary infection the virus persists in a latent form in the host tissues invading the immune system.
- Reactivation can occur in response to inflammatory stimuli, physiologic stress and immunosuppression releasing new virions that can infect new cells causing cmv end organ infection.
- T-cells play a role in controlling the replication of the virus.
- In patients with T-cell deficiency the viral replication is uncontrolled and results in excessive shedding of the virus.
- Reactivation of the virus results in the release of cytokines such as TNF-α and IFN-γ resulting in inflammation.
Genetics
- Patients with polymorphisms in the genes coding for mannose binding lectin and ficolin-2 are at a higher risk of developing CMV infection.[7]
Associated Conditions
- Symptomatic cytomegalovirus is associated with HIV infection in majority of patients.[8][9]
Microscopic Pathology
- CMV infection demonstrates the presence of intranuclear inclusion bodies. These inclusion bodies stain dark pink on an H&E stain, and are also called "Owl's Eye" inclusion bodies.
References
- ↑ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. pp. 556, 566–9. ISBN 0838585299.
- ↑ Staras SAS, Dollard SC, Radford KW; et al. (2006). "Seroprevalence of cytomegalovirus infection in the United States, 1988–1994". Clin Infect Dis. 43: 1143&ndash, 51. PMID 17029132.
- ↑ Goodman AL, Murray CD, Watkins J, Griffiths PD, Webster DP (2015). "CMV in the gut: a critical review of CMV detection in the immunocompetent host with colitis". Eur J Clin Microbiol Infect Dis. 34 (1): 13–8. doi:10.1007/s10096-014-2212-x. PMC 4281362. PMID 25097085.
- ↑ Rafailidis PI, Mourtzoukou EG, Varbobitis IC, Falagas ME (2008). "Severe cytomegalovirus infection in apparently immunocompetent patients: a systematic review". Virol J. 5: 47. doi:10.1186/1743-422X-5-47. PMC 2289809. PMID 18371229.
- ↑ Khan TV, Toms C (2016). "Cytomegalovirus Colitis and Subsequent New Diagnosis of Inflammatory Bowel Disease in an Immunocompetent Host: A Case Study and Literature Review". Am J Case Rep. 17: 538–43. PMC 4968430. PMID 27460032.
- ↑ Einbinder Y, Wolf DG, Pappo O, Migdal A, Tsvang E, Ackerman Z (2008). "The clinical spectrum of cytomegalovirus colitis in adults". Aliment Pharmacol Ther. 27 (7): 578–87. doi:10.1111/j.1365-2036.2008.03595.x. PMID 18194509.
- ↑ Klenerman P, Oxenius A (2016). "T cell responses to cytomegalovirus". Nat Rev Immunol. 16 (6): 367–77. doi:10.1038/nri.2016.38. PMID 27108521.
- ↑ Grønborg HL, Jespersen S, Hønge BL, Jensen-Fangel S, Wejse C (2017). "Review of cytomegalovirus coinfection in HIV-infected individuals in Africa". Rev Med Virol. 27 (1). doi:10.1002/rmv.1907. PMID 27714898.
- ↑ Gianella S, Letendre S (2016). "Cytomegalovirus and HIV: A Dangerous Pas de Deux". J Infect Dis. 214 Suppl 2: S67–74. doi:10.1093/infdis/jiw217. PMC 5021239. PMID 27625433.