Salivary gland virus is the former name of Cytomegalovirus (CMV). They belong to the group of herpes virus of humans and animals. They lead to prolonged latency in infected hosts.
CMV is the largest virus of the herpes family. They exhibit strict host specificity and infection. They have been identified in humans, monkeys and guinea pigs.
CMV is unrelated to other herpes viruses based on antigens. They are characterized by the enlargement of infected cells. The name ‘cytomegalia’ was given because of this enlargement caused.
In neonates and immunodeficient, they cause severe disseminated disease. Self limiting diseases are visualized in children and normal adults and may be asymptomatic.
The CMV disease is very rare, but the infection with the virus is common. In most of the cases, the infections are not clear, leading to a prolonged latent period with occasional reactivation. Clinical disease may be caused due to intrauterine or postnatal infections.
Intrauterine diseases lead to the death of the fetus or cause cytomegalic inclusion disease of the newborn, which is fatal. Jaundice, hemolytic anemia, enlarged spleen, inflammation of the retina, calcification of the cerebrum, etc., are other manifestations that may be associated with it. Mental retardation may follow.
In infants, the skin may become yellow, birth weight may be reduced, pneumonia, purple colored rashes on the skin, etc., may be seen.
Fever, pneumonia, diarrhea, hepatitis, bleeding digestive tract ulcers, blindness and even coma are seen in immunocompromised.
Cytomegalic inclusion disease is seen exclusively seen in infants with mothers showing primary CMV infection during pregnancy. Perinatal infection may be acquired from the mother through genital secretions or breast milk. Primary infection in older children and adults are asymptomatic.
In immune compromised individuals, CMV causes fatal and severe infections. This occurs generally in transplant recipients, cancer patients on chemotherapy, and more particularly in HIV infected ones.
It is an important, when AIDS patients are concerned. In AIDS patients, the already weakened immune system was damaged further by CMV by inhibiting the non- specific cell mediated immunity. Irrelevant immunoglobulins mask the attached viral particle, thereby escaping the anti-CMV antibody.
Diagnosis may be established when the virus is recovered from urine, saliva or other body fluids. Simpler, but less reliable method is to demonstrate cytomegalic cells in the centrifuged deposits from urine or saliva.
Primary infection may be detected by the demonstration of antibody, but ineffective in the cases of reactivation. Serological diagnosis such as ELISA, Immunofluorescence, Complement Fixation test, etc.,  may be used. Antibody detection should be done before donating organ or blood.
Spread:
1. Spreads slowly with close contact
2. Spread through saliva, other secretion or sexual contact.
3. Blood transfusion and organ transplant also spread the disease
4. Virus has been detected in milk, saliva, semen, blood, urine and cervical secretions.
5. Infants shed virus in urine up to 4- 5 years.
6. Once infected, the person carries the virus forever.
Acyclovir is used in the prophylaxis, but not in treatment. Ganciclovir and foscarnet are effective and used in the treatment of CMV disease in AIDS patients.
No vaccines are available. Experimentally, live attenuated vaccines (Towne 125 and AD 169 strains) and a purified CMV polypeptide vaccine have been found to be immunogenic but not effective in immunodeficient subjects from CMV infections.