Pathogenesis and Pathology of Cytomegalovirus
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p489-491
2025-11-16
51
A. Normal Hosts
CMV may be transmitted from person to person in several different ways, all requiring close contact with virus-bearing material. There is a 4- to 8-week incubation period in nor mal older children and adults after viral exposure. The virus causes a systemic infection; it has been isolated from lung, liver, esophagus, colon, kidneys, monocytes, and T and B lymphocytes. The disease can manifest as an infectious mononucleosis-like syndrome, although most CMV infections are subclinical. Similar to all herpesviruses, CMV establishes lifelong latent infections. Virus can be shed intermittently from the pharynx and in the urine for months to years after primary infection (Figure 1). Prolonged CMV infection of the kidney does not seem to be deleterious in nor mal persons. Salivary gland involvement is common and is probably chronic.
Fig1. Clinical, virologic, and immunologic features of cytomegalovirus infection in normal individuals (A) and in congenitally infected infants (B). Ab, antibody; Ag, antigen; CF, complement fixing; CMV, cytomegalovirus; CNS, central nervous system; Ig, immunoglobulin; LTR, lymphocyte transformation response; Nt, neutralizing. (Reproduced with permission from Alford CA, Britt WJ: Cytomegalovirus. In Fields BN, Knipe DM [editors-in-chief]. Virology, 2nd ed. Raven Press, 1990.)
Cell-mediated immunity is depressed with primary infections (see Figure 1), and this may contribute to the persistence of viral infection. It may take several months for cellular responses to recover.
B. Immunosuppressed Hosts
Primary CMV infections in immunosuppressed hosts are much more severe than in normal hosts. Individuals at greatest risk for CMV disease are those receiving hemapoietic stem cell and solid organ transplants, those with malignant tumors who are receiving chemotherapy, and those with AIDS. Viral excretion is increased and prolonged, and the infection is more apt to become disseminated. Pneumonia and colitis are the most common complications.
The host immune response presumably maintains CMV in a latent state in seropositive individuals. Reactivated infections are associated with disease much more often in immunocompromised patients than in normal hosts. Although usually less severe, reactivated infections may be as virulent as primary infections.
C. Congenital and Perinatal Infections
Fetal and newborn infections with CMV may be severe (Figure 2). About 1% of live births annually in the United States have congenital CMV infections, and about 5–10% of those will develop severe cytomegalic inclusion dis ease. A high percentage of babies with this disease will exhibit developmental defects and mental retardation.
Fig2. Congenital infections by cytomegalovirus and birth defects in symptomatic and asymptomatic children. Cytomegalovirus is the most common intrauterine infection associated with congenital defects. (Reproduced with permission from Pereira L, Maidji E, McDonagh S, Tabata T: Insights into viral transmission at the uterine-placental interface. Trends Microbiol 2005;13:164–174. Copyright Elsevier.)
The virus can be transmitted in utero with both primary and reactivated maternal infections. About one-third of pregnant women with primary infection transmit the virus. Generalized cytomegalic inclusion disease results most often from primary maternal infections. There is no evidence that gestational age at the time of maternal infection affects expression of disease in the fetus. Intrauterine transmission occurs in about 1% of seropositive women. Fetal damage seldom results from these reactivated maternal infections; the infection of the infant remains subclinical though chronic (see Figure 1).
CMV can also be acquired by the infant from exposure to virus in the mother’s genital tract during delivery and from maternal breast milk. In these cases, the infants usually have received some maternal antibody, and the perinatally acquired CMV infections tend to be subclinical. Transfusion acquired CMV infections in newborns vary, depending on the amount of virus received and the serologic status of the blood donor. Whether CMV is acquired in utero or perinatally, viral shedding is more prolonged than when the virus is acquired later in life (see Figure 1).
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