Cytomegalovirus infection pathophysiology: Difference between revisions
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===Transmission=== | ===Transmission=== | ||
*Transmission of CMV occurs from person to person. | *Transmission of CMV occurs from person to person. | ||
* [[Seroprevalence]] is age-dependent: 58.9% of individuals aged 6 and over are infected with CMV while 90.8% of individuals aged 80 and over are positive for CMV.<ref>{{cite journal | author=Staras SAS, Dollard SC, Radford KW, ''et al.'' | title=Seroprevalence of cytomegalovirus infection in the United States, 1988–1994 | year=2006 | journal=Clin Infect Dis | volume=43 | pages=1143–51 | pmid = 17029132}}</ref> Infection requires close, intimate contact with a person excreting the virus in their [[saliva]], [[urine]], [[blood]], [[tears]], and [[semen]]. | * [[Seroprevalence]] is age-dependent: 58.9% of individuals aged 6 and over are infected with CMV while 90.8% of individuals aged 80 and over are positive for CMV.<ref>{{cite journal | author=Staras SAS, Dollard SC, Radford KW, ''et al.'' | title=Seroprevalence of cytomegalovirus infection in the United States, 1988–1994 | year=2006 | journal=Clin Infect Dis | volume=43 | pages=1143–51 | pmid = 17029132}}</ref> | ||
*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. | *The shedding of virus may take place intermittently, without any detectable signs, and without causing symptoms. | ||
*CMV can be [[Sexually transmitted disease|sexually transmitted]] and can also be transmitted via [[Breastfeeding|breast milk]], transplanted organs, and rarely from [[blood transfusion]]s. | *CMV can be [[Sexually transmitted disease|sexually transmitted]] and can also be transmitted via [[Breastfeeding|breast milk]], transplanted organs, and rarely from [[blood transfusion]]s. | ||
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Following transmission, the primary infection is usually asymptomatic in immunocompetent individuals. Latency state develops after the primary infection in immunocompetent individuals with CMV infection persisting in the host tissues by evading the immune system. Reactivation of the infection occurs in persons with latent CMV when the host's immune system becomes compromised. CMV usually colonizes inflamed tissues than healthy tissues. Cytokines such as TNF-α and IFN-γ, are released following local inflammation in the bowel wall. CMV gets to the mucosa of the colon through the macrophages. The cytokines reactivate latent CMV infection and promote the migration of CMV-infected macrophages to inflamed colon. This further causes damage to the tissue.<ref>{{cite journal | author=Staras SAS, Dollard SC, Radford KW, ''et al.'' | title=Seroprevalence of cytomegalovirus infection in the United States, 1988–1994 | year=2006 | journal=Clin Infect Dis | volume=43 | pages=1143–51 | pmid = 17029132}}</ref><ref name="pmid25097085">{{cite journal| author=Goodman AL, Murray CD, Watkins J, Griffiths PD, Webster DP| title=CMV in the gut: a critical review of CMV detection in the immunocompetent host with colitis. | journal=Eur J Clin Microbiol Infect Dis | year= 2015 | volume= 34 | issue= 1 | pages= 13-8 | pmid=25097085 | doi=10.1007/s10096-014-2212-x | pmc=4281362 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25097085 }} </ref><ref name="pmid18371229">{{cite journal| author=Rafailidis PI, Mourtzoukou EG, Varbobitis IC, Falagas ME| title=Severe cytomegalovirus infection in apparently immunocompetent patients: a systematic review. | journal=Virol J | year= 2008 | volume= 5 | issue= | pages= 47 | pmid=18371229 | doi=10.1186/1743-422X-5-47 | pmc=2289809 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18371229 }} </ref><ref name="pmid27460032">{{cite journal| author=Khan TV, Toms C| title=Cytomegalovirus Colitis and Subsequent New Diagnosis of Inflammatory Bowel Disease in an Immunocompetent Host: A Case Study and Literature Review. | journal=Am J Case Rep | year= 2016 | volume= 17 | issue= | pages= 538-43 | pmid=27460032 | doi= | pmc=4968430 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27460032 }} </ref><ref name="pmid18194509">{{cite journal| author=Einbinder Y, Wolf DG, Pappo O, Migdal A, Tsvang E, Ackerman Z| title=The clinical spectrum of cytomegalovirus colitis in adults. | journal=Aliment Pharmacol Ther | year= 2008 | volume= 27 | issue= 7 | pages= 578-87 | pmid=18194509 | doi=10.1111/j.1365-2036.2008.03595.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18194509 }} </ref> | Following transmission, the primary infection is usually asymptomatic in immunocompetent individuals. Latency state develops after the primary infection in immunocompetent individuals with CMV infection persisting in the host tissues by evading the immune system. Reactivation of the infection occurs in persons with latent CMV when the host's immune system becomes compromised. CMV usually colonizes inflamed tissues than healthy tissues. Cytokines such as TNF-α and IFN-γ, are released following local inflammation in the bowel wall. CMV gets to the mucosa of the colon through the macrophages. The cytokines reactivate latent CMV infection and promote the migration of CMV-infected macrophages to inflamed colon. This further causes damage to the tissue.<ref>{{cite journal | author=Staras SAS, Dollard SC, Radford KW, ''et al.'' | title=Seroprevalence of cytomegalovirus infection in the United States, 1988–1994 | year=2006 | journal=Clin Infect Dis | volume=43 | pages=1143–51 | pmid = 17029132}}</ref><ref name="pmid25097085">{{cite journal| author=Goodman AL, Murray CD, Watkins J, Griffiths PD, Webster DP| title=CMV in the gut: a critical review of CMV detection in the immunocompetent host with colitis. | journal=Eur J Clin Microbiol Infect Dis | year= 2015 | volume= 34 | issue= 1 | pages= 13-8 | pmid=25097085 | doi=10.1007/s10096-014-2212-x | pmc=4281362 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25097085 }} </ref><ref name="pmid18371229">{{cite journal| author=Rafailidis PI, Mourtzoukou EG, Varbobitis IC, Falagas ME| title=Severe cytomegalovirus infection in apparently immunocompetent patients: a systematic review. | journal=Virol J | year= 2008 | volume= 5 | issue= | pages= 47 | pmid=18371229 | doi=10.1186/1743-422X-5-47 | pmc=2289809 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18371229 }} </ref><ref name="pmid27460032">{{cite journal| author=Khan TV, Toms C| title=Cytomegalovirus Colitis and Subsequent New Diagnosis of Inflammatory Bowel Disease in an Immunocompetent Host: A Case Study and Literature Review. | journal=Am J Case Rep | year= 2016 | volume= 17 | issue= | pages= 538-43 | pmid=27460032 | doi= | pmc=4968430 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27460032 }} </ref><ref name="pmid18194509">{{cite journal| author=Einbinder Y, Wolf DG, Pappo O, Migdal A, Tsvang E, Ackerman Z| title=The clinical spectrum of cytomegalovirus colitis in adults. | journal=Aliment Pharmacol Ther | year= 2008 | volume= 27 | issue= 7 | pages= 578-87 | pmid=18194509 | doi=10.1111/j.1365-2036.2008.03595.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18194509 }} </ref> | ||
===Genetics=== | ===Genetics=== | ||
As a result of efforts to create an [[attenuated virus]] [[vaccine]], there currently exist two general classes of CMV. | As a result of efforts to create an [[attenuated virus]] [[vaccine]], there currently exist two general classes of CMV. | ||
Revision as of 14:44, 16 May 2017
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Cytomegalovirus infection Microchapters |
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Differentiating Cytomegalovirus infection from other Diseases |
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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
Pathophysiology
Transmission
- Transmission of CMV occurs from person to person.
- Seroprevalence is age-dependent: 58.9% of individuals aged 6 and over are infected with CMV while 90.8% of individuals aged 80 and over are positive for CMV.[1]
- 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.
- Although CMV is not highly contagious, it has been shown to spread in households and among young children in day care centers.[2]
Following transmission, the primary infection is usually asymptomatic in immunocompetent individuals. Latency state develops after the primary infection in immunocompetent individuals with CMV infection persisting in the host tissues by evading the immune system. Reactivation of the infection occurs in persons with latent CMV when the host's immune system becomes compromised. CMV usually colonizes inflamed tissues than healthy tissues. Cytokines such as TNF-α and IFN-γ, are released following local inflammation in the bowel wall. CMV gets to the mucosa of the colon through the macrophages. The cytokines reactivate latent CMV infection and promote the migration of CMV-infected macrophages to inflamed colon. This further causes damage to the tissue.[3][4][5][6][7]
Genetics
As a result of efforts to create an attenuated virus vaccine, there currently exist two general classes of CMV.
- Clinical isolates comprise those viruses obtained from patients and represent the wild type viral genome.
- Laboratory strains have been cultured extensively in the lab setting and typically contain numerous accumulated mutations. Most notably, the laboratory strain AD169 appears to lack a 15kb region of the 200kb genome that is present in clinical isolates. This region contains 19 open reading frames whose functions have yet to be elucidated. AD169 is also unique in that it is unable to enter latency and nearly always assumes lytic growth upon infection.
Species
| Name | Abv. | Host |
|---|---|---|
| Cercopithecine herpesvirus 5 | (CeHV-5) | African green monkey |
| Cercopithecine herpesvirus 8 | (CeHV-8) | Rhesus monkey |
| Human herpesvirus 5 | (HHV-5) | Humans |
| Pongine herpesvirus 4 | (PoHV-4) | ? |
| Aotine herpesvirus 1 | (AoHV-1) | (Tentative species) |
| Aotine herpesvirus 3 | (AoHV-3) | (Tentative species) |
Associated Conditions
Specific disease entities recognised in immunocompromised people with CMV infection are cytomegalovirus retinitis (inflammation of the retina, characterised by a "pizza pie appearance" on ophthalmoscopy) and cytomegalovirus colitis (inflammation of the large bowel).
Microscopic Pathology
Microscopically, CMV can be demonstrated by intranuclear inclusion bodies, which show that the virus replicates in the nucleus rather than the cytosol. These inclusion bodies stain dark pink on an H&E stain, and are also called "Owl's Eye" inclusion bodies.
Lytically replicating virus disrupts the cytoskeleton, causing massive cell enlargement, which is the source of the virus' name.
References
- ↑ 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.
- ↑ 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.