Cytomegalovirus infection pathophysiology
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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
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.