Expression of measles virus RNA in peripheral blood mononuclear cells of patients with measles, SSPE, and autoimmune diseases

Schneider-Schaulies, S.; Kreth, Hans Wolfgang; Hofmann, G.; Billeter, Martin; Meulen, Volker ter

doi:10.1016/0042-6822(91)90611-e

Cited by 45 publications

(22 citation statements)

References 21 publications

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“…One study using a cloned probe [114] indicated by dot blot the presence of MV RNA in 28 out of 34 SLE patients and not in 29 controls. A study using the more sensitive S1 nuclease protection assay was not able to confirm the presence of MV-specific RNA in the PBMCs of SLE patients [115]. However, to the best of our knowledge, RT/PCR has not yet been applied.…”

Section: Systemic Lupus Erythematosismentioning

confidence: 77%

Morbilliviruses and human disease

Rima

Duprex

2005

The Journal of Pathology

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Morbilliviruses are a group of viruses that belong to the family Paramyxoviridae. The most instantly recognizable member is measles virus (MV) and individuals acutely infected with the virus exhibit a wide range of clinical symptoms ranging from a characteristic mild selflimiting infection to death. Canine distemper virus (CDV) and rinderpest virus (RPV) cause a similar but distinctive pathology in dogs and cattle, respectively, and these, alongside experimental MV infection of primates, have been useful models for MV pathogenesis. Traditionally, viruses were identified because a distinctive disease was observed in man or animals; an infectious agent was subsequently isolated, cultured, and this could be used to recapitulate the disease in an experimentally infected host. Thus, satisfying Koch's postulates has been the norm. More recently, particularly due to the advent of exceedingly sensitive molecular biological assays, many researchers have looked for infectious agents in disease conditions for which a viral aetiology has not been previously established. For these cases, the modified Koch's postulates of Bradford Hill have been developed as criteria to link a virus to a specific disease. Only in a few cases have these conditions been fulfilled. Therefore, many viruses have over the years been definitely and tentatively linked to human diseases and in this respect the morbilliviruses are no different. In this review, human diseases associated with morbillivirus infection have been grouped into three broad categories: (1) those which are definitely caused by the infection; (2) those which may be exacerbated or facilitated by an infection; and (3) those which currently have limited, weak, unsubstantiated or no credible scientific evidence to support any link to a morbillivirus. Thus, an attempt has been made to clarify the published data and separate human diseases actually linked to morbilliviruses from those that are merely anecdotally associated.

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Section: Systemic Lupus Erythematosismentioning

confidence: 77%

Morbilliviruses and human disease

Rima

Duprex

2005

The Journal of Pathology

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“…The spontaneous proliferation of mononuclear cells sampled from the peripheral blood of infected individuals occurs just before the rash appears and persists for several weeks (39, 42), providing multiple targets for productive MV infection (131). Nevertheless, MV infects only a small proportion of circulating PBMC in the infected host (49,96,116,135), and the major cell type infected in vivo seems to be in the monocyte/macrophage lineage (29).…”

Section: Proposed Mechanisms Of MV Immunosuppressionmentioning

confidence: 99%

Immune Containment and Consequences of Measles Virus Infection in Healthy and Immunocompromised Individuals

Permar

Griffin

Letvin

2006

Clin Vaccine Immunol

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2The pathogenicity of measles virus (MV) is intimately linked to the immune status of the infected individual. Measles is typically a self-limiting disease; however, individuals who are immunocompromised (56,79), malnourished (26,78,113), or at the extremes of age (23) are at increased risk for severe measles. At the present time, with human immunodeficiency virus (HIV) and immunosuppressive drug therapy affecting the immune competence of large numbers of individuals, MV is reemerging as an important pathogen worldwide. Elucidating the mechanism by which the immune system controls MV infection and prevents reinfection will be crucial for our understanding of disease pathogenesis and transmission as well as the development of novel MV vaccination strategies.Despite reaching global measles vaccination coverage of Ͼ80% of individuals, MV remains the fifth leading cause of death and the most common cause of vaccine-preventable death in children under 5 years of age (84). An estimated 31 million cases of measles occurred globally in 2001, resulting in 777,000 deaths, the majority (452,000) of which occurred in sub-Saharan Africa (84). MV is one of the most contagious pathogens known to humans, and large measles outbreaks, facilitated by overcrowding in poor communities, continue to occur even in countries that have achieved high vaccine coverage.MV is a 15-kilobase, enveloped, negative-strand RNA virus and a member of the Morbillivirus genus of the Paramyxoviridae family. MV infects only humans and nonhuman primates. It is a stable, monotypic virus, making it an excellent candidate for eventual eradication. In culture, MV can be adapted to grow in nonprimate cells, a process that has facilitated the attenuation of viral strains for the development of a safe vaccine. Measles is transmitted via direct person-to-person contact and causes a symptomatic viral prodrome culminating in the hallmark maculopapular measles rash. The measles rash is preceded by systemic viremia and lymphopenia, and clearance of the rash is followed by a transient suppression of T-lymphocyte responses that lasts several weeks, leaving the infected individual susceptible to other infections.While nonspecific innate immune mechanisms may be important in the control of MV during the first days following infection, adaptive MV-specific immune responses mediate viral clearance and provide protection against subsequent MV infections. Natural MV infection generates long-lasting immunity that includes both MV-specific antibody (14) and memory T-lymphocyte (50, 123, 136) responses. Long-term protection from reinfection occurs without a requirement for reexposure (98).This article reviews our current understanding of the immune control of MV and the consequences of MV infection on the immune system of the immunocompetent host. We then discuss the clinical consequences of MV infection in immunocompromised individuals. Finally, we describe recent studies that have raised questions regarding the outcome of MV infection in the immunocompromised host. IMMUNE CO...

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“…The tropism of MV for cells of the lymphocytic and monocytic lineage is well established both in vivo and in vitro (Esolen et al, 1993 ;Schneider-Schaulies et al, 1991 ;Joseph et al, 1975) ; particularly, MV infection interferes with the proliferation and generation of specialized lymphocyte functions in vitro, but not with those already established prior to infection (Galama et al, 1980 ;Yanagi et al, 1992 ;McChesney et al, 1987McChesney et al, , 1988. Detailed analyses revealed that MV infection caused an arrest in the G " phase of the cell cycle in these cells (Yanagi et al, 1992 ;McChesney et al, 1987McChesney et al, , 1988.…”

Section: Introductionmentioning

confidence: 99%

Measles virus-induced immunosuppression in vitro is associated with deregulation of G1 cell cycle control proteins.

Engelking

Fedorov

Lilischkis

et al. 1999

Journal of General Virology

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Virus-induced immunosuppression is the major cause of the high morbidity/mortality rates associated with acute measles. It has been shown previously that mitogen-dependent proliferation of peripheral blood lymphocytes (PBL) was strongly impaired after contact with the measles virus (MV) glycoproteins F and H expressed on the surface of infected cells, cells transfected with the corresponding expression constructs or UV-inactivated MV (UV-MV). The state of unresponsiveness was not associated with the induction of apoptosis, and a significant proportion of PBL was found to be arrested in the G 0 /G 1 phase of the cell cycle. It is now shown that cell cycle cessation, rather than complete arrest, is induced after MV glycoprotein contact. No obvious role was found for p53 in the induction of this unresponsiveness. With UV-MV as effector, downregulation of p27, an inhibitor of cyclin-dependent kinase (CDK)-cyclin complexes, was significantly delayed after mitogenic stimulation of human PBL. The activities of both CDK4/6-cyclin D and CDK2-cyclin E complexes for phosphorylation of exogenous substrates in vitro were strongly reduced. CDK4, CDK6, cyclins D3 and E and, to a minor extent, CDK2 failed to accumulate at the protein level after mitogenic stimulation in the presence of UV-MV. These data indicate that MV-induced proliferative unresponsiveness of PBL to mitogenic stimulation is associated with a drastic deregulation of the expression of cell cycle genes essential for the G 1 /S phase transition.

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Expression of measles virus RNA in peripheral blood mononuclear cells of patients with measles, SSPE, and autoimmune diseases

Cited by 45 publications

References 21 publications

Morbilliviruses and human disease

Morbilliviruses and human disease

Immune Containment and Consequences of Measles Virus Infection in Healthy and Immunocompromised Individuals

Measles virus-induced immunosuppression in vitro is associated with deregulation of G1 cell cycle control proteins.

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