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Classification and external resources
Specialty infectious disease
ICD-10 B25
ICD-9-CM 078.5
MedlinePlus 000568
Patient UK Cytomegalovirus
MeSH D003586
Cytomegalovirus 01.jpg
Typical "owl eye" inclusion indicating CMV infection of a lung pneumocyte[1]
Virus classification
Group: Group I (dsDNA)
Order: Herpesvirales
Family: Herpesviridae
Subfamily: Betaherpesvirinae
Genus: Cytomegalovirus
Type species
Human cytomegalovirus
Main article: Human cytomegalovirus

Cytomegalovirus (from the Greek cyto-, "cell", and megalo-, "large") is a genus of viruses in the order Herpesvirales, in the family Herpesviridae, in the subfamily Betaherpesvirinae. Human and monkeys serve as natural hosts. There are currently eight species in this genus including the type species human herpesvirus 5. Diseases associated with HHV-5 include mononucleosis, and pneumonias.[2][3] It is typically abbreviated as CMV.

The species that infects humans is commonly known as human CMV (HCMV) or human herpesvirus-5 (HHV-5), and is the most studied of all cytomegaloviruses.[4] Within Herpesviridae, CMV belongs to the Betaherpesvirinae subfamily, which also includes the genera Muromegalovirus and Roseolovirus (HHV-6 and HHV-7).[5] It is related to other herpesviruses within the subfamilies of Alphaherpesvirinae that includes herpes simplex viruses (HSV)-1 and -2 and varicella-zoster virus (VZV), and the Gammaherpesvirinae subfamily that includes Epstein–Barr virus.[4]

All herpesviruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals.[5] Other CMV viruses are found in several mammal species, but species isolated from animals differ from HCMV in terms of genomic structure, and have not been reported to cause human disease.


Group: dsDNA



Classified Cytomegaloviruses
Scientific Name Host Common Name

Human herpesvirus 5 (HHV-5)
Cercopithecine herpesvirus 5 (CeHV-5)
Cercopithecine herpesvirus 8 (CeHV-8)
Panine herpesvirus 2 (PoHV-2)
Pongine herpesvirus 4 (PoHV-4)
Aotine herpesvirus 1 (AoHV-1)—tentative classification
Aotine herpesvirus 3 (AoHV-3)—tentative classification

African green monkey
Rhesus monkey
Night monkey

Human CMV (HCMV)
Simian CMV (SCCMV)
Rhesus CMV (RhCMV)
Chimpanzee CMV (CCMV)
Herpesvirus aotus 1
Herpesvirus aotus 3

Several species of Cytomegalovirus have been identified and classified for different mammals.[5] The most studied is Human cytomegalovirus (HCMV), which is also known as Human herpesvirus 5 (HHV-5). Other primate CMV species include Chimpanzee cytomegalovirus (CCMV) that infects chimpanzees and orangutans, and Simian cytomegalovirus (SCCMV) and Rhesus cytomegalovirus (RhCMV) that infect macaques; CCMV is known as both Panine herpesvirus 2 (PaHV-2) and Pongine herpesvirus-4 (PoHV-4). SCCMV is called Cercopithecine herpesvirus-5 (CeHV-5) and RhCMV, Cercopithecine herpesvirus 8 (CeHV-8). A further two viruses found in the night monkey are tentatively placed in the Cytomegalovirus genus, and are called Herpesvirus aotus 1 and Herpesvirus aotus 3. Rodents also have viruses previously called cytomegaloviruses that are now reclassified under the genus Muromegalovirus; this genus contains Mouse cytomegalovirus (MCMV) is also known as Murid herpesvirus 1 (MuHV-1) and the closely related Murid herpesvirus 2 (MuHV-2) that is found in rats. In addition, there many other viral species with the name Cytomegalovirus identified in distinct mammals that are as yet not completely classified; these were predominantly isolated from primates and rodents.


Viruses in Cytomegalovirus are enveloped, with icosahedral, Spherical to pleomorphic, and Round geometries, and T=16 symmetry. The diameter is around 150-200 nm. Genomes are linear and non-segmented, around 200kb in length.[2]

Genus Structure Symmetry Capsid Genomic Arrangement Genomic Segmentation
Cytomegalovirus Spherical Pleomorphic T=16 Enveloped Linear Monopartite

Life Cycle[edit]

Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved by attachment of the viral glycoproteins to host receptors, which mediates endocytosis. Replication follows the dsDNA bidirectional replication model. DNA templated transcription, with some alternative splicing mechanism is the method of transcription. Translation takes place by leaky scanning. The virus exits the host cell by nuclear egress, and budding. Human and monkeys serve as the natural host. Transmission routes are contact, urine, and saliva.[2]

Genus Host Details Tissue Tropism Entry Details Release Details Replication Site Assembly Site Transmission
Cytomegalovirus Humans; monkeys Epithelial mucosa Glycoprotiens Budding Nucleus Nucleus Urine; saliva


Main article: Human cytomegalovirus

Human cytomegalovirus is a species of virus that belongs to the viral family known as Herpesviridae or herpesviruses. It is typically abbreviated as HCMV and is alternatively known as Human herpesvirus 5 (HHV-5).[4] Within Herpesviridae, HCMV belongs to the Betaherpesvirinae subfamily, which also includes cytomegaloviruses from other mammals.[5]

Although they may be found throughout the body, HCMV infections are frequently associated with the salivary glands.[5] HCMV infection is typically unnoticed in healthy people, but can be life-threatening for the immunocompromised, such as HIV-infected persons, organ transplant recipients,[6] or new born infants.[4] It can cause hydrops fetalis in infants. After infection, HCMV has an ability to remain latent within the body over long periods. CMV persists in the host because the viral genome encodes multiple proteins that interfere with MHC class I presentation of viral antigens. One viral protein blocks translocation of peptides into the lumen of the endoplasmic reticulum, while two other viral proteins cause degradation of MHC class I proteins before they reach the cell surface.[7] Hence, diagnosis is done histologically by looking for inclusion bodies in salivary glands. A prevention by hygienic measures is included in information given to pregnant women.[8]

HCMV is found throughout all geographic locations and socioeconomic groups, and infects between 50% and 80% of adults in the United States (>90% worldwide[9]) as indicated by the presence of antibodies in a majority of the general population.[4] Seroprevalence is age-dependent: 58.9% of individuals aged 6 and older are infected with CMV while 90.8% of individuals aged 80 and older are positive for HCMV.[10] HCMV infection during pregnancy results in transmission to a developing fetus. Between 0.2% and 2% of newborns are infected in studies that have been carried out worldwide. HCMV infection occurs earlier in life and is more widespread in developing countries and, in developed countries, in communities with lower socioeconomic status. HCMV represents the most significant infectious cause of birth defects in industrialized countries. Congenital HCMV "infection is the leading infectious cause of deafness, learning disabilities, and mental retardation in children."[11] CMV infection may also "have a large impact on immune parameters in later life and may contribute to increased morbidity and eventual mortality."[12]


Main article: human cytomegalovirus

Need for vaccine to protect pregnant women[edit]

A vaccine against HCMV is currently under investigation. As a member of the TORCH complex, cytomegalovirus can cause congenital infection and disease, primarily sensorineural hearing loss. HCMV is the primary infectious cause of hearing loss recognized at birth, which has focused development of a vaccine to protect pregnant women. Development of such a vaccine has been emphasized as a priority by the National Vaccine Program Office in the United States. A phase 2 study of a CMV vaccine published in 2009 indicated an efficacy of 50%, with limited durability. Thus the protection provided was limited and a number of subjects contracted CMV infection despite the vaccination. In one case also congenital CMV was encountered, although there were fewer transplacental transmissions in the vaccinated groups than in the control group.[13]


  1. ^ Mattes FM, McLaughlin JE, Emery VC, Clark DA, Griffiths PD (August 2000). "Histopathological detection of owl's eye inclusions is still specific for cytomegalovirus in the era of human herpesviruses 6 and 7". J. Clin. Pathol. 53 (8): 612–4. doi:10.1136/jcp.53.8.612. PMC 1762915. PMID 11002765. 
  2. ^ a b c "Viral Zone". ExPASy. Retrieved 15 June 2015. 
  3. ^ a b ICTV. "Virus Taxonomy: 2014 Release". Retrieved 15 June 2015. 
  4. ^ a b c d e Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 556; 566–9. ISBN 0-8385-8529-9. 
  5. ^ a b c d e Koichi Yamanishi; Arvin, Ann M.; Gabriella Campadelli-Fiume; Edward Mocarski; Moore, Patrick; Roizman, Bernard; Whitley, Richard (2007). Human herpesviruses: biology, therapy, and immunoprophylaxis. Cambridge, UK: Cambridge University Press. ISBN 0-521-82714-0. 
  6. ^ Gandhi MK, Khanna R (December 2004). "Human cytomegalovirus: clinical aspects, immune regulation, and emerging treatments". Lancet Infect Dis 4 (12): 725–38. doi:10.1016/S1473-3099(04)01202-2. PMID 15567122. 
  7. ^ Emmanuel J.H.J Wiertz, Thomas R Jones, Lei Sun, Matthew Bogyo, Hans J Geuze and Hidde L Ploegh. (1996). "The Human Cytomegalovirus US11 Gene Product Dislocates MHC Class I Heavy Chains from the Endoplasmic Reticulum to the Cytosol" (PDF). Cell 84 (5): 769–779. doi:10.1016/S0092-8674(00)81054-5. PMID 8625414. 
  8. ^ Guitton, Sébastien. "Information on congenital CMV". 
  9. ^ Mocarski ES, Shenk T, Griffiths P, Pass RF (2013). Fields Virology (6th ed.). Lippincott Williams & Wilkins. pp. 1960–2014. ISBN 9780781736473. 
  10. ^ Staras SA, Dollard SC, Radford KW, Flanders WD, Pass RF, Cannon MJ (November 2006). "Seroprevalence of cytomegalovirus infection in the United States, 1988–1994". Clin. Infect. Dis. 43 (9): 1143–51. doi:10.1086/508173. PMID 17029132. 
  11. ^ Elizabeth G. Damato and Caitlin W. Winnen (2006). "Cytomegalovirus infection: perinatal implications". J Obstet Gynecol Neonatal Nurs 31 (1): 86–92. doi:10.1111/j.1552-6909.2002.tb00026.x. PMID 11843023. 
  12. ^ Caruso C, Buffa S, Candore G et al. (2009). "Mechanisms of immunosenescence" (PDF). Immun Ageing 6: 10. doi:10.1186/1742-4933-6-10. PMC 2723084. PMID 19624841. 
  13. ^ Pass RF, Zhang C, Evans A et al. (2009). "Vaccine prevention of maternal cytomegalovirus infection". N Engl J Med 360 (12): 1191–9. doi:10.1056/NEJMoa0804749. PMC 2753425. PMID 19297572. 

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