Viral Persistence: Chronic and Latent Virus Infections
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 , p442-443
2025-10-28
57
Infections are acute when a virus first infects a susceptible host. Viral infections are usually self-limiting, but some may persist for long periods of time in the host. Long-term virus host interaction may take several forms. Chronic infections (also called persistent infections) are those in which replicating virus can be continuously detected, often at low levels; mild or no clinical symptoms may be evident. Latent infections are those in which the virus persists in an occult (hidden or cryptic) form most of the time when no new virus is produced. There can be intermittent flare-ups of clinical dis ease; infectious virus can be recovered during these times. Viral sequences may be detectable by molecular techniques in tissues harboring latent infections. Inapparent or subclinical infections are those that give no overt sign of their presence.
Chronic infections occur with a number of animal viruses, and the persistence in certain instances depends on the age of the host when infected. In humans, for example, rubella virus and CMV infections acquired in utero characteristically result in viral persistence that is of limited duration, probably because of development of the immunologic capacity to react to the infection as the infant matures. Infants infected with hepatitis B virus frequently become persistently infected (chronic carriers); most carriers are asymptomatic.
Herpesviruses typically produce latent infections. HSVs enter the sensory ganglia and persist in a noninfectious state (Figure 1). There may be periodic reactivations during which lesions containing infectious virus appear at peripheral sites (eg, fever blisters). Chickenpox virus (varicella-zoster) also becomes latent in sensory ganglia. Recurrences are rare and occur years later, usually following the distribution of a peripheral nerve (shingles). Other members of the herpesvirus family also establish latent infections, including CMV and EBV. All may be reactivated by immunosuppression. Consequently, reactivated herpesvirus infections may be a serious complication for persons receiving immunosuppressant therapy.
Fig1. Latent infections by herpesviruses. Examples are shown for both herpes simplex and varicella-zoster viruses. Primary infections occur in childhood or adolescence, followed by establishment of latent virus in the cerebral or spinal ganglia. Later activation causes recurrent herpes simplex or zoster. CMI, cell-mediated immunity. (Modified from Mims CA, White DO: Viral Pathogenesis and Immunology. Copyright © 1984 by Blackwell Science Ltd. With permission from Wiley.)
Persistent viral infections play a far-reaching role in human disease. Persistent viral infections are associated with certain types of cancers in humans as well as with progressive degenerative diseases of the CNS of humans. Examples of different types of persistent viral infections are presented in Figure2.
Fig2. Different types of virus–host interactions: apparent (clinical disease), inapparent (subclinical), chronic, latent, occult, and slow infections. (1) Measles runs an acute, almost always clinically apparent course resulting in long-lasting immunity. (2) Measles may also be associated with persistence of latent infection in subacute sclerosing panencephalitis (see Chapter 40). (3) Yellow fever and influenza follow a pattern similar to that of measles except that infection may be more often subclinical than clinical. (4) In hepatitis B, recovery from clinical disease may be associated with chronic infection in which fully active virus persists in the blood. (5) Some infections are, in a particular species, always subclinical, such as eastern equine encephalomyelitis (EEE) in some species of birds that then act as reservoirs of the virus. (6) For human papillomavirus, the course of infection is chronic; when cervical cancer develops, the virus present is occult (not replicating). (7) Infection of humans with certain adenoviruses may be clinical or subclinical. There may be a long latent infection during which virus is present in small quantity; virus may also persist after the illness. (8) The periodic reactivation of latent HSV, which may recur throughout life in humans, often follows an initial acute episode of stomatitis in childhood. (9) Infection may be unrecognized for long periods of time before it becomes apparent. Examples of such “slow” infections characterized by long incubation periods are scrapie in sheep and kuru in humans (caused by prions, not viruses). (10) In pigs that have eaten virus-bearing lungworms, swine “flu” is occult until the appropriate stimulus induces viral production and, in turn, clinical disease. (11) Lymphocytic choriomeningitis (LCM) virus may be established in mice by in utero infection. A form of immunologic tolerance develops in which virus-specific T cells are not activated. Antibody is produced against viral proteins; this antibody and circulating LCM virus form antigen–antibody complexes that produce immune complex disease in the host. The presence of LCM virus in this chronic infection (circulating virus with little or no apparent disease) may be revealed by transmission to an indicator host (eg, adult mice from a virus-free stock). (12) All adult mice develop classic acute symptoms of LCM and frequently die. (13) The possibility is shown of infection with an occult virus that is not detectably replicating. Proof of the presence of such a virus remains a difficult task that, however, is attracting the attention of cancer investigators.
Spongiform encephalopathies are a group of chronic, progressive, fatal infections of the CNS caused by unconventional, transmissible agents called prions. Prions are not viruses, but are proteins whose structural alterations can cause conformational changes in host proteins leading to aggregation and dysfunction, and are transmissible similar to other infectious agents. Some examples of prion infections are scrapie in sheep, bovine spongiform encephalopathy in cattle, and kuru and Creutzfeldt-Jakob disease in humans.
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