MHC class I immune evasion in MCMV infection

Doom, Carmen M.; Hill, Ann B.

doi:10.1007/s00430-008-0089-y

Cited by 62 publications

(49 citation statements)

References 78 publications

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“…We chose time points as late as 3 to 4 mo after primary infection when MCMV latency is established (39). Notably, Lanier and co-workers (12) had recently proposed that expansion of NK cell subsets would lead to a form of "NK cell memory."…”

Section: Nk Cell Proliferation In Latent MCMV Infectionmentioning

confidence: 99%

Genetic Labeling Reveals Altered Turnover and Stability of Innate Lymphocytes in Latent Mouse Cytomegalovirus Infection

Busche

Schmitz

Fleige

et al. 2011

The Journal of Immunology

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Mouse CMV (MCMV) infection rapidly induces the proliferation of NK cells, which correlates with immunological protection. Whether NK cells primed during acute response against MCMV are maintained for the long term is not known. In this study, we used TcrdH2BeGFP mice in which maturing NK cells are genetically labeled with a pulse of very stable histone-2B–eGFP. In this system, we found that the reporter protein was diluted out upon NK cell division during acute MCMV infection. At the same time, mature NK cells in uninfected mice showed only very limited turnover in vivo. Three months after primary infection when MCMV latency was established, the majority of peripheral NK cells still displayed a higher record of proliferation than NK cells in mock-infected controls. This observation included both Ly49H+ and Ly49H– NK cells. Conversely, naive NK cells did not show more proliferation after transfer into latently MCMV-infected mice than that after transfer into mock-infected control mice. This indicated that the observed alterations of the NK cell compartment in MCMV latency were “legacy” (i.e., resulting from prior events during the initial immune response). Together, these results suggest that antiviral immune responses induce sustained alterations of innate lymphocyte populations that extend far beyond the first days of acute infection.

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Section: Nk Cell Proliferation In Latent MCMV Infectionmentioning

confidence: 99%

Genetic Labeling Reveals Altered Turnover and Stability of Innate Lymphocytes in Latent Mouse Cytomegalovirus Infection

Busche

Schmitz

Fleige

et al. 2011

The Journal of Immunology

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“…Surprisingly, little is known about the natural route of infection by MCMV. While intranasal MCMV infection of adult mice has been used occasionally in previous studies (Jordan, 1978;Shanley et al, 1997;Morello et al, 2005), the only effort to systematically compare it with other routes of infection relied on low infection doses and was limited in its interpretation because of wide variations of outcomes between cages (Doom and Hill, 2008). A study on a model of neonate mouse infection reported that a transgenic MCMV, expressing mCherry as a reporter gene, could be found in the lungs of neonates infected by the laryngopharyngeal route and in adult mice infected intranasally (i.n.)…”

Section: Introductionmentioning

confidence: 99%

Murine cytomegalovirus (CMV) infection via the intranasal route offers a robust model of immunity upon mucosal CMV infection

Oduro

Redeker

Lemmermann

et al. 2016

Journal of General Virology

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Cytomegalovirus (CMV) is a ubiquitous virus, causing the most common congenital infection in humans, yet a vaccine against this virus is not available. Experimental studies of immunity against CMV in animal models of infection, such as the infection of mice with mouse CMV (MCMV), have relied mainly on parenteral infection protocols, although the virus naturally transmits by mucosal routes via body fluids. To characterize the biology of infections by mucosal routes, we compared the kinetics of virus replication, latent viral load and CD8 T-cell responses in lymphoid organs upon experimental intranasal (targeting the respiratory tract) and intragastric (targeting the digestive tract) infection with systemic intraperitoneal infection of two unrelated mouse strains. We observed that intranasal infection induced robust and long-term virus replication in the lungs and salivary glands but limited replication in the spleen. CD8 T-cell responses were somewhat weaker than upon intraperitoneal infection but showed similar kinetic profiles and phenotypes of antigen-specific cells. In contrast, intragastric infection resulted in abortive or poor virus replication in all tested organs and poor T-cell responses to the virus, especially at late times after infection. Consistent with the T-cell kinetics, the MCMV latent load was high in the lungs but low in the spleen of intranasally infected mice and lowest in all tested organs upon intragastric infection. In conclusion, we showed that intranasal but not intragastric infection of mice with MCMV represents a robust model to study the short-and long-term biology of CMV infection by a mucosal route.

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“…Cross-presentation may play a fundamental role in the induction of antiviral CD8 1 T-cell responses in situations where viruses encode for proteins that directly interfere with the antigen presentation machinery of infected cells. Murine cytomegalovirus (MCMV) expresses proteins that directly target MHC and costimulatory molecules in infected APCs [8][9][10][11]. Despite such impressive immune evasion, strong CD8 1 T-cell responses are induced upon MCMV infection, suggesting that cross-presentation may play an important role [12].…”

Section: Introductionmentioning

confidence: 99%

Batf3 transcription factor‐dependent DC subsets in murine CMV infection: Differential impact on T‐cell priming and memory inflation

Torti¹,

Walton²,

Murphy³

et al. 2011

Eur J Immunol

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Priming of CD81 T cells specific for viruses that interfere with the MHC class I presentation pathway is a challenge for the immune system and is believed to rely on cross-presentation. Cytomegalovirus (CMV) infection induces vigorous CD8 1 T-cell responses despite its potent immune evasion strategies. Furthermore, CD8 1 T cells specific for a subset of viral epitopes accumulate and are maintained at high levels exhibiting an activated phenotype -referred to as ''inflationary T cells''. Taking advantage Batf3 À/À mice in which the development of cross-presenting CD8a 1 and CD103 1 DCs is severely compromised, we analyzed their role in the induction and inflation of murine (M)CMV-specific CD8 1 T-cell responses. We found that priming of MCMV-specific CD8 1 T cells was severely impaired in the absence of cross-presenting DCs. However, inflation of two immuno-dominant MCMVspecific CD8 1 T-cell populations was largely normal in the absence of cross-presenting DCs, indicating that inflation during latency was mainly dependent on direct antigen presentation. These results highlight differential antigen presentation requirements during acute and latent MCMV infection.

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MHC class I immune evasion in MCMV infection

Cited by 62 publications

References 78 publications

Genetic Labeling Reveals Altered Turnover and Stability of Innate Lymphocytes in Latent Mouse Cytomegalovirus Infection

Genetic Labeling Reveals Altered Turnover and Stability of Innate Lymphocytes in Latent Mouse Cytomegalovirus Infection

Murine cytomegalovirus (CMV) infection via the intranasal route offers a robust model of immunity upon mucosal CMV infection

Batf3 transcription factor‐dependent DC subsets in murine CMV infection: Differential impact on T‐cell priming and memory inflation

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