Measles virus-induced immunosuppression: from effectors to mechanisms

Avota, Elita; Gassert, Evelyn; Schneider‐Schaulies, Sibylle

doi:10.1007/s00430-010-0152-3

Cited by 53 publications

(39 citation statements)

References 119 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Another concern is that viruses such as Rift Valley fever virus (RVFV) or Nairobi sheep disease virus (NSDV) may replicate preferentially in PPRaffected animals. MeV infection has been shown to cause profound immune suppression as a result of lymphopenia, cytokine imbalances and deficient expansion of PBMCs [66]. Immune suppression was also seen in RPV-infected animals, even those exposed only to the vaccine [67].…”

Section: Development and Application Of Pprv Vaccinesmentioning

confidence: 99%

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Baron

Diop

Njeumi

et al. 2017

Journal of General Virology

View full text Add to dashboard Cite

Peste des petits ruminants virus (PPRV) is a significant pathogen of small ruminants and is prevalent in much of Africa, the Near and Middle East and Asia. Despite the availability of an efficacious and cheap live-attenuated vaccine, the virus has continued to spread, with its range stretching from Morocco in the west to China and Mongolia in the east. Some of the world's poorest communities rely on small ruminant farming for subsistence and the continued endemicity of PPRV is a constant threat to their livelihoods. Moreover, PPRV's effects on the world's population are felt broadly across many economic, agricultural and social situations. This far-reaching impact has prompted the Food and Agriculture Organization of the United Nations (FAO) and the World Organisation for Animal Health (OIE) to develop a global strategy for the eradication of this virus and its disease. PPRV is a morbillivirus and, given the experience of these organizations in eradicating the related rinderpest virus, the eradication of PPRV should be feasible. However, there are many critical areas where basic and applied virological research concerning PPRV is lacking. The purpose of this review is to highlight areas where new research could be performed in order to guide and facilitate the eradication programme. These areas include studies on disease transmission and epidemiology, the existence of wildlife reservoirs and the development of next-generation vaccines and diagnostics. With the support of the international virology community, the successful eradication of PPRV can be achieved.

show abstract

Section: Development and Application Of Pprv Vaccinesmentioning

confidence: 99%

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Baron

Diop

Njeumi

et al. 2017

Journal of General Virology

View full text Add to dashboard Cite

show abstract

“…For example, deaths from pneumococcal disease often occur in the wake of influenza (35). Virus-induced immunosuppression may be long-lasting and underlie a broader susceptibility, as exemplified by measles (36). Other viruses, such as the HIV, weaken immunity in a more sustained and profound manner (37).…”

Section: Acquired Immunodeficiencymentioning

confidence: 99%

Human genetic basis of interindividual variability in the course of infection

Casanova

2015

Proc. Natl. Acad. Sci. U.S.A.

160

111

View full text Add to dashboard Cite

The key problem in human infectious diseases was posed at the turn of the 20th century: their pathogenesis. For almost any given virus, bacterium, fungus, or parasite, life-threatening clinical disease develops in only a small minority of infected individuals. Solving this infection enigma is important clinically, for diagnosis, prognosis, prevention, and treatment. Some microbes will inevitably remain refractory to, or escape vaccination, or chemotherapy, or both. The solution also is important biologically, because the emergence and evolution of eukaryotes alongside more rapidly evolving prokaryotes, archaea, and viruses posed immunological challenges of an ecological and evolutionary nature. We need to study these challenges in natural, as opposed to experimental, conditions, and also at the molecular and cellular levels. According to the human genetic theory of infectious diseases, inborn variants underlie life-threatening infectious diseases. Here I review the history of the field of human genetics of infectious diseases from the turn of the 19th century to the second half of the 20th century. This paper thus sets the scene, providing the background information required to understand and appreciate the more recently described monogenic forms of resistance or predisposition to specific infections discussed in a second paper in this issue.

show abstract

“…Importantly, even though wild-type and vaccine MV strains have been extensively studied at the levels of virulence (55), immunosuppression, and immune response (4,21,36) and the crystal structures of CD46 and SLAM receptor binding to MV hemagglutinin have recently been elucidated (7,17,41), there are still few data about the roles of the CD46 and SLAM receptors in the process of MV entry. Furthermore, although MV is thought to enter the cell by pH-independent fusion at the plasma membrane, recent findings with other paramyxoviruses, like Nipah virus, raise the possibility of macropinocytosis as an entry route (35).…”

mentioning

confidence: 99%

Measles Virus Glycoprotein-Pseudotyped Lentiviral Vector-Mediated Gene Transfer into Quiescent Lymphocytes Requires Binding to both SLAM and CD46 Entry Receptors

Frecha

Lévy

Costa

et al. 2011

J Virol

View full text Add to dashboard Cite

Gene transfer into quiescent T and B cells is of importance for gene therapy and immunotherapy approaches to correct hematopoietic disorders. Previously, we generated lentiviral vectors (LVs) pseudotyped with the Edmonston measles virus (MV) hemagglutinin and fusion glycoproteins (Hgps and Fgps) (H/F-LVs), which, for the first time, allowed efficient transduction of quiescent human B and T cells. These target cells express both MV entry receptors used by the vaccinal Edmonston strain, CD46 and signaling lymphocyte activation molecule (SLAM). Interestingly, LVs pseudotyped with an MV Hgp, blind for the CD46 binding site, were completely inefficient for resting-lymphocyte transduction. Similarly, SLAM-blind H mutants that recognize only CD46 as the entry receptor did not allow stable LV transduction of resting T cells. The CD46-tropic LVs accomplished vector-cell binding, fusion, entry, and reverse transcription at levels similar to those achieved by the H/F-LVs, but efficient proviral integration did not occur. Our results indicate that both CD46 and SLAM binding sites need to be present in cis in the Hgp to allow successful stable transduction of quiescent lymphocytes. Moreover, the entry mechanism utilized appears to be crucial: efficient transduction was observed only when CD46 and SLAM were correctly engaged and an entry mechanism that strongly resembles macropinocytosis was triggered. Taken together, our results suggest that although vector entry can occur through the CD46 receptor, SLAM binding and subsequent signaling are also required for efficient LV transduction of quiescent lymphocytes to occur.Measles virus (MV) belongs to the paramyxoviridae family and is the causative agent of measles disease. It has two envelope glycoproteins (gp's), the hemagglutinin (H) and fusion (F) glycoproteins (Hgp and Fgp, respectively), which mediate receptor binding and fusion, respectively (28, 29). Signaling lymphocyte activation molecule (SLAM) (CD150) is the receptor for both clinical isolates and vaccine strains (49, 55). However, vaccine strains like Edmonston (Edm) have gained, in addition to entry through the SLAM receptor, entry through the CD46 receptor after their adaptation in SLAM-negative cells (25,54). Moreover, recent findings suggest the existence of a third MV receptor in epithelial cells (54). CD46 is a complementregulatory molecule expressed on all human nucleated cells (27), whereas SLAM is constitutively expressed at the surfaces of some T and B cell subsets and upregulated upon proliferation of T and B lymphocytes and mature dendritic cells (DCs) (3,8). The cellular distribution of SLAM determines lymphoid tropism and explains in part the immunosuppressive character of measles virus.Importantly, even though wild-type and vaccine MV strains have been extensively studied at the levels of virulence (55), immunosuppression, and immune response (4, 21, 36) and the crystal structures of CD46 and SLAM receptor binding to MV hemagglutinin have recently been elucidated (7,17,41), there are still few data abo...

show abstract

Measles virus-induced immunosuppression: from effectors to mechanisms

Cited by 53 publications

References 119 publications

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Human genetic basis of interindividual variability in the course of infection

Measles Virus Glycoprotein-Pseudotyped Lentiviral Vector-Mediated Gene Transfer into Quiescent Lymphocytes Requires Binding to both SLAM and CD46 Entry Receptors

Contact Info

Product

Resources

About