Everything about Human Herpesvirus 5 totally explained
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Cytomegalovirus (CMV) (from the
Greek cyto-, "cell", and
-megalo-, "large") is a
viral genus of the
Herpesviruses group: in humans it's commonly known as HCMV or
Human Herpesvirus 5 (HHV-5). CMV belongs to the
Betaherpesvirinae subfamily of
Herpesviridae, which also includes
Roseolovirus. Other herpesviruses fall into the subfamilies of
Alphaherpesvirinae (including
HSV 1 and 2 and
varicella) or
Gammaherpesvirinae (including
Epstein-Barr virus). HCMV is also the
virus most frequently transmitted to a developing child before birth. HCMV
infection is more widespread in developing countries and in communties with lower socioeconomic status and represents the most significant viral cause of birth defects in industrialized countries.
Species
Pathogenesis
Most healthy people who are infected by HCMV after birth have no symptoms. with prolonged
fever, and a mild
hepatitis. A sore throat is common. After infection, the virus remains latent in the body for the rest of the person's life. Overt disease rarely occurs unless
immunity is suppressed either by drugs, infection or old-age. Initial HCMV infection, which often is
asymptomatic is followed by a prolonged, inapparent infection during which the virus resides in cells without causing detectable damage or clinical illness.
Infectious CMV may be shed in the bodily fluids of any infected person, and can be found in
urine,
saliva,
blood,
tears,
semen, and
breast milk. The
shedding of virus can occur intermittently, without any detectable signs or symptoms.
CMV infection can be demonstrated microscopically by the detection of intranuclear
inclusion bodies. The inclusion bodies stain dark pink by
H&E staining, and are called "Owl's Eye" inclusion bodies.
HCMV infection is important to certain high-risk groups. Major areas of risk of infection include
pre-natal or
post-partum infants and
immunocompromised individuals, such as
organ transplant recipients, persons with
leukemia, or those infected with human immunodeficiency virus (
HIV). HCMV is considered an
AIDS-defining infection, indicating that the
T-cell count has dropped to low levels.
Lytically replicating virus disrupts the
cytoskeleton, causing massive cell enlargement, which is the source of the virus' name.
Transmission and prevention
Transmission of HCMV occurs from person to person through bodily fluids. Infection requires close, intimate contact with a person excreting the virus in their saliva, urine, or other bodily fluids. CMV can be
sexually transmitted and can also be transmitted via
breast milk, transplanted organs, and rarely from
blood transfusions.
Although HCMV isn't highly contagious, it has been shown to spread in households and among young children in day care centers. Between 22-38% of infected foetuses are then born with symptoms, which may include pneumonia, gastrointestinal, retinal and neurological disease. HCMV infection occurs in roughly 1% of all neonates with those who are not congenitally infected contracting the infection possibly through breast milk. Other sources of neonatal infection are bodily fluids which are known to contain high titres in shedding individuals: Saliva (<10
7copies/ml) and urine (<10
5copies/ml ) seem common routes of transmission.
The incidence of primary CMV infection in pregnant women in the United States varies from 1% to 3%. Healthy pregnant women are not at special risk for disease from CMV infection. When infected with CMV, most women have no symptoms and very few have a disease resembling mononucleosis. It is their developing fetuses that may be at risk for congenital CMV disease. CMV remains the most important cause of congenital viral infection in the United States. HCMV is the most common cause of congenital infection in humans and intrauterine primary infections are second only to Down's syndrome as a known cause of mental retardation.
For infants who are infected by their mothers before birth, two potential adverse scenarios exist:
- Generalized infection may occur in the infant, and can cause complications such as low birth weight, microcephaly, seizures, petechial rash similar to the "blueberry muffin" rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice). Though severe cases can be fatal, with supportive treatment most infants with CMV disease will survive. However, from 80% to 90% will have complications within the first few years of life that may include hearing loss, vision impairment, and varying degrees of mental retardation.
- Another 5% to 10% of infants who are infected but without symptoms at birth will subsequently have varying degrees of hearing and mental or coordination problems.
However, these risks appear to be almost exclusively associated with women who previously have not been infected with CMV and who are having their first infection with the virus during pregnancy. Even in this case, two-thirds of the infants won't become infected, and only 10% to 15% of the remaining third will have symptoms at the time of birth. There appears to be little risk of CMV-related complications for women who have been infected at least 6 months prior to conception. For this group, which makes up 50% to 80% of the women of child-bearing age, the rate of newborn CMV infection is 1%, and these infants appear to have no significant illness or abnormalities.
Treatment
No treatment is generally necessary for CMV infection in the healthy individual since the majority of infections resolve on their own. Antiviral drug therapy is now being evaluated in infants.
Ganciclovir treatment is used for patients with depressed immunity who have either sight-related or life-threatening illnesses.
Valganciclovir (marketed as Valcyte) is an antiviral drug that's also effective and is given orally. The therapeutic effectiveness is frequently compromised by the emergence of drug-resistant virus isolates. A variety of amino acid changes in the UL97 protein kinase and the viral DNA polymerase have been reported to cause drug resistance.
Foscarnet or cidofovir can be given in patients with CMV resistant to ganciclovir, because foscarnet has bad nephrotoxicity, increased or decreased Ca2+ or P, and decreased Mg2+.
Vaccines are still in the research and development stage.
Genomics
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's 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's unable to enter latency and nearly always assumes lytic growth upon infection.Further Information
Get more info on 'Human Herpesvirus 5'.
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