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See detailA gammaherpesvirus licenses CD8 T cells to protect the host from pneumovirus-induced immunopathologies.
Dourcy, Mickael ULiege; Maquet, Céline ULiege; Dams, Lorène ULiege et al

in Mucosal Immunology (2020)

Human respiratory syncytial virus (RSV) is a pneumovirus that causes severe infections in infants worldwide. Despite intensive research, safe and effective vaccines against RSV have remained elusive. The ... [more ▼]

Human respiratory syncytial virus (RSV) is a pneumovirus that causes severe infections in infants worldwide. Despite intensive research, safe and effective vaccines against RSV have remained elusive. The main reason is that RSV infection of children previously immunized with formalin-inactivated-RSV vaccines has been associated with exacerbated pathology, a phenomenon called RSV vaccine-enhanced respiratory disease. In parallel, despite the high RSV prevalence, only a minor proportion of children develop severe diseases. Interestingly, variation in the immune responses against RSV or following RSV vaccination could be linked with differences of exposure to microbes during childhood. Gammaherpesviruses (γHVs), such as the Epstein–Barr virus, are persistent viruses that deeply influence the immune system of their host and could therefore affect the development of pneumovirus-induced immunopathologies for the long term. Here, we showed that a previous ɣHV infection protects against both pneumovirus vaccine-enhanced disease and pneumovirus primary infection and that CD8 T cells are essential for this protection. These observations shed a new light on the understanding of pneumovirus-induced diseases and open new perspectives for the development of vaccine strategies. [less ▲]

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See detailHelminth infection is associated with the accumulation of lung interstitial macrophages and increased susceptibility to γ-herpesvirus infection in C57BL/6 mice
Rolot, Marion; Preure, Amira ULiege; Dougall, Annette et al

Scientific conference (2020, March 06)

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See detailUnconventional CD45RA+ memory CD8 T cells to control HIV infection during antiretroviral therapy.
Rolot, Marion; Dewals, Benjamin G ULiege

in Cellular & molecular immunology (2020)

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See detailHelminth infection is associated with the accumulation of lung interstitial macrophages and increased susceptibility to gammaherpesvirus infection in C57BL/6 mice
Rolot, Marion; Preure, Amira; Dougall, Annette et al

Conference (2019, December 02)

Parasitic helminths can condition innate cells such as lung macrophages for accelerated clearance in a secondary infection. However, it is unknown how helminth-induced macrophage changes in the lung ... [more ▼]

Parasitic helminths can condition innate cells such as lung macrophages for accelerated clearance in a secondary infection. However, it is unknown how helminth-induced macrophage changes in the lung affect the response to concurrent bystander infection with viruses. Here, we have examined the lung macrophage responses after Schistosoma mansoni egg-induced inflammation or Nippostrongylus brasiliensis infection and observed a severe accumulation of CD11b+ interstitial macrophages (IntMs) while siglec-F+ alveolar macrophages (AlvMs) were reduced. Interestingly, expansion of IntMs was more pronounced in C57BL/6 compared to BALB/c mice and we observed a strong upregulation of the M(IL-4) alternative activation marker YM1 in IntMs of C57BL/6, compared to BALB/c mice. We then examined the susceptibility of both mouse strains to murid gammaherpesvirus 4 (MuHV-4) infection and observed that helminth exposure rendered C57BL/6 mice highly susceptible to MuHV-4 acute infection whereas BALB/c mice controlled viral infection earlier as previously published by our group through the expansion of “virtual” memory CD8+ T cells (Tvm) (Rolot et al., 2018. Nat Commun. 2018 Oct 30;9(1):4516). We further confirmed the role of IL-4-induced Tvm in the CD8-mediated control of MuHV-4 in both C57BL/6 and BALB/c strains, suggesting that the increased early susceptibility of C57BL/6 mice to MuHV-4 does not affect the induction of effector CD8+ T cells. Finally, we observed increased proportions of MuHV-4-infected macrophages after 4 days post-infection when C57BL/6 mice were exposed to helminths, suggesting that helminth infection modifies the lung macrophage niche to become more permissive to MuHV-4 infection. [less ▲]

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See detailHelminth-induced interleukin 4 expands bystander memory T cells for early control of viral infection
Dewals, Benjamin G ULiege

Conference (2019, December)

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8+ T cells (TVM) are non-conventional T cells displaying memory ... [more ▼]

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8+ T cells (TVM) are non-conventional T cells displaying memory properties that can be generated through responsiveness to interleukin (IL)-4. However, it is not clear if helminth-induced type 2 immunity functionally affects the TVMcompartment. Here, we show that helminths expand CD44hiCD62LhiCXCR3hiCD49dlo TVM cells through direct IL-4 signaling in CD8+ T cells. Importantly, helminth-mediated conditioning of TVMcells provided enhanced control of acute respiratory infection with the murid gammaherpesvirus 4 (MuHV-4). This enhanced control of MuHV-4 infection could further be explained by an increase in antigen-specific CD8+ T cell effector responses in the lung and was directly dependent on IL-4 signaling. These results demonstrate that IL-4 during helminth infection can non-specifically condition CD8+ T cells, leading to a subsequently raised antigen-specific CD8+ T cell activation that enhances control of viral infection. [less ▲]

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See detailHelminth infection is associated with expansion of lung interstitial macrophages and increased susceptibility to gammaherpesvirus infection in C57BL/6 mice
Rolot, Marion; Preure, Amira; Dougall, Annette et al

Conference (2019, June 24)

Exposure to parasitic helminths can imprint the immune system to modulate bystander immune responses to viral infection. We have recently shown that IL-4 induced during helminth infection expand bystander ... [more ▼]

Exposure to parasitic helminths can imprint the immune system to modulate bystander immune responses to viral infection. We have recently shown that IL-4 induced during helminth infection expand bystander “virtual” memory CD8+ T cells (TVM) that results in enhanced control of murid gammaherpesvirus 4 (MuHV-4) lytic infection in the lung (Rolot et al., 2018. Nat Commun. 2018 Oct 30;9(1):4516). Whereas the frequency of TVM in secondary lymphoid organs in homeostasis is known to be higher in Balb/c compared to C57BL/6 mice, we observed here that IL-4c treatment or helminth exposure induced TVM expansion and enhanced CD8-mediated control of MuHV-4 in both strains. However, lung exposure to helminths in C57BL/6 mice resulted in severely increased viral loads after MuHV-4 infection. Such increased susceptibility to MuHV-4 infection was restricted to the strain C57BL/6 and was observed after induction of Schistosoma mansoni egg-induced lung inflammation and after Nippostrongylus brasiliensis infection. Following viral respiratory infection, MuHV-4 virions are first licensed by lung macrophages to infect alveolar epithelial cells, suggesting that macrophage responses could be affected by helminth-induced inflammation. Interestingly, helminth exposure induced a severe expansion of CD11b+ interstitial macrophages displaying M(IL-4) polarisation with increased Relm-α, PD-L2 and MHC-II expression. In addition, we observed increased proportions of MuHV-4-infected macrophages when C57BL/6 mice were exposed to helminths. Altogether, these results suggest that helminth infection affects the lung macrophages which become more permissive to MuHV-4 infection. [less ▲]

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See detailThe Critical Role of Genome Maintenance Proteins in Immune Evasion During Gammaherpesvirus Latency
Sorel, Océane ULiege; Dewals, Benjamin G ULiege

in Frontiers in Microbiology (2019), 9(3315),

Gammaherpesviruses are important pathogens that establish latent infection in their natural host for lifelong persistence. During latency, the viral genome persists in the nucleus of infected cells as a ... [more ▼]

Gammaherpesviruses are important pathogens that establish latent infection in their natural host for lifelong persistence. During latency, the viral genome persists in the nucleus of infected cells as a circular episomal element while the viral gene expression program is restricted to non-coding RNAs and a few latency proteins. Among these, the genome maintenance protein (GMP) is part of the small subset of genes expressed in latently infected cells. Despite sharing little peptidic sequence similarity, gammaherpesvirus GMPs have conserved functions playing essential roles in latent infection. Among these functions, GMPs have acquired an intriguing capacity to evade the cytotoxic T cell response through self-limitation of MHC class I-restricted antigen presentation, further ensuring virus persistence in the infected host. In this review, we provide an updated overview of the main functions of gammaherpesvirus GMPs during latency with an emphasis on their immune evasion properties. [less ▲]

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See detailPre-conception maternal helminth infection transfers via nursing long-lasting cellular immunity against helminths to offspring
Darby, M. G.; Chetty, A.; Mrjden, D. et al

in Science Advances (2019), 5(5),

Maternal immune transfer is the most significant source of protection from early-life infection, but whether maternal transfer of immunity by nursing permanently alters offspring immunity is poorly ... [more ▼]

Maternal immune transfer is the most significant source of protection from early-life infection, but whether maternal transfer of immunity by nursing permanently alters offspring immunity is poorly understood. Here, we identify maternal immune imprinting of offspring nursed by mothers who had a pre-conception helminth infection. Nursing of pups by helminth-exposed mothers transferred protective cellular immunity to these offspring against helminth infection. Enhanced control of infection was not dependent on maternal antibody. Protection associated with systemic development of protective type 2 immunity in T helper 2 (TH2) impaired IL-4R-/- offspring. This maternally acquired immunity was maintained into maturity and required transfer (via nursing) to the offspring of maternally derived TH2-competent CD4 T cells. Our data therefore reveal that maternal exposure to a globally prevalent source of infection before pregnancy provides long-term nursing-acquired immune benefits to offspring mediated by maternally derived pathogen-experienced lymphocytes. © 2019 by the Authors. [less ▲]

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See detailRecruitment of hepatic macrophages from monocytes is independent of IL-4Ralpha but is associated with ablation of resident macrophages in schistosomiasis.
Rolot, Marion ULiege; Dougall, Annette; Javaux, Justine et al

in European journal of immunology (2019)

Alternatively-activated Mphis (AAMphi) accumulate in hepatic granulomas during schistosomiasis and have been suggested to originate in the bone marrow. What is less understood is how these Mphi responses ... [more ▼]

Alternatively-activated Mphis (AAMphi) accumulate in hepatic granulomas during schistosomiasis and have been suggested to originate in the bone marrow. What is less understood is how these Mphi responses are regulated after S. mansoni infection. Here, we investigated the role of IL-4 receptor alpha-chain (IL-4Ralpha)-signalling in the dynamics of liver Mphi responses. We observed that IL-4Ralpha signalling was dispensable for the recruitment of Ly6C(hi) monocytes and for their conversion into F4/80(hi) CD64(hi) CD11b(hi) Mphi. Moreover, while IL-4Ralpha provided an AAMphi phenotype to liver F4/80(hi) CD64(hi) CD11b(hi) Mphi that was associated with regulation of granuloma formation, it was dispensable for host survival. Resident F4/80(hi) CD64(hi) CD11b(lo) Mphi did not upregulate the AAMphi signature gene Ym1. Rather, resident Mphi nearly disappeared by week 8 after infection and artificial ablation of resident Mphi in CD169(DTR) mice did not affect the response to S. mansoni infection. Interestingly, ablation of CD169(+) cells in naive mice resulted in the accumulation of F4/80(hi) CD64(hi) CD11b(hi) Mphi, which was amplified when ablation occurred during schistosomiasis. Altogether, our results suggest the ablation of resident KCs after S. mansoni infection to be associated with the recruitment and accumulation of F4/80(hi) CD64(hi) CD11b(hi) Mphi with lyz2-dependent IL-4Ralpha contributing to the regulation of granuloma inflammation but being dispensable for host survival. This article is protected by copyright. All rights reserved. [less ▲]

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See detailParasitic infections and maternal immunity.
Horsnell, William; Dewals, Benjamin G ULiege

in Parasite Immunology (2019), 41(3), 12615

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See detailRNA-seq analysis of latently-infected CD8+ T lymphocytes during bovine malignant catarrhal fever reveals unconventional TCR cell activation
Myster, Françoise ULiege; Javaux, Justine ULiege; Van Campe, Willem et al

Conference (2018, December 20)

Alcelaphine herpesvirus 1 (AlHV-1) persists in wildebeest asymptomatically but induces malignant catarrhal fever (MCF) upon transmission to other ruminant species, including cattle. We have previously ... [more ▼]

Alcelaphine herpesvirus 1 (AlHV-1) persists in wildebeest asymptomatically but induces malignant catarrhal fever (MCF) upon transmission to other ruminant species, including cattle. We have previously shown that MCF is a lethal disease resembling a peripheral T cell lymphoma (PTCL) and induced after ORF73-dependent latency establishment in CD8+ T lymphocytes. However, how AlHV-1 infection leads to CD8+ T lymphocyte proliferation and activation remains largely unknown. In this study, we investigated viral and cellular transcriptomes of bovine CD8+ T lymphocytes during MCF. Three groups of four 4-month-old calves were mock-infected or infected intranasally with 105 PFU of the virulent C500 wildtype (WT) strain or non-pathogenic ORF73-deficient (73null) AlHV-1 strain. At day 45 after infection (mock and 73null groups) or at time of MCF development (WT group), CD8+ T lymphocytes were isolated from peripheral blood to high purity before RNA extraction. Illumina Truseq stranded mRNA libraries were obtained and subjected to NextSeq500 sequencing. Transcriptomes were analysed for both viral and cellular transcripts. We took advantage of the non-pathogenic 73null strain to differentiate anti-viral effector/memory responses in CD8+ T cells from transcriptomics changes due to latent infection of these cells during MCF. While no viral transcripts could be detected in CD8+ T cells of mock or 73null-infected animals, expression of viral genes of interest in MCF-developing calves was detected including AlHV-1-specific semaphorin-like A3, undefined A4, bZIP protein A6, interleukin 4-like protein A9.5 and undefined glycoprotein A10. When analysing differential cellular gene expression (P < 10−4; change in expression of over fourfold), we observed upregulation of 151 (WT vs Mock) and 72 (WT vs 73null) genes, including Gzma, SerpinB9, Moxd1, Tox2, IL-10, and Cxcr3; and downregulation of 205 (WT vs Mock) and 271 (WT vs 73null) genes, including αv or β3 integrins. Intriguingly, while gene-set enrichment for TCR engagement was observed in CD8+ T cells from MCF-developing calves, supporting T cell activation, we also observed strong downregulation of gene transcripts normally involved in canonical TCR activation such as Cbl, Tec family tyrosine kinases Rlk, Tec, and Itk, and Syk. These data suggest unconventional TCR triggering and provide unprecedented mechanistic insights on how AlHV-1 could induce a PTCL-like disease. Future work should further determine the actual pathway(s) involved and which viral gene(s) drive T cell dysregulation. [less ▲]

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See detailLyz2-specific deletion of IL-4 receptor alpha chain in schistosomiasis does not preclude Ly6Chigh monocytes as the main source of liver macrophages but impairs alternative activation and increase inflammation
Rolot, Marion; Dougall, Annette; Javaux, Justine et al

Conference (2018, September 24)

M(IL-4) accumulate in liver granulomas of Schistosoma mansoni-infected mice from recruited Ly6Chi monocytes and modulate inflammation. Here, we used conditional IL-4 receptor α-chain (IL-4Rα) knockdown ... [more ▼]

M(IL-4) accumulate in liver granulomas of Schistosoma mansoni-infected mice from recruited Ly6Chi monocytes and modulate inflammation. Here, we used conditional IL-4 receptor α-chain (IL-4Rα) knockdown Il4ra−/loxlyz2Cre mice to determine whether impairing M(IL-4) modifies the dynamics of Mφ responses in liver granulomas after S. mansoni infection. First, we used reporter RosatdRFP mice crossed with lyz2Cre mice to validate selective Cre-mediated excision in neutrophils and Mφ in naive and S. mansoni infected mice. Next, the liver inflammatory responses were investigated during the first weeks of S. mansoni infection. We observed significantly increased total leukocyte numbers, including monocytes, in the liver by week 8 in Il4ra−/loxlyz2Cre mice while these mice survived the infection similarly to hemizygous Il4ra−/lox mice. When investigating liver monocyte/Mφ responses, we observed that CD11blo resident Küpffer cells (KCs) were severely reducing in term of number over the course of infection and independently of IL-4Rα signalling. While KCs lowered, Ly6Chi monocytes were recruited as soon as week 4 and strongly proliferated by week 8 pi. We further observed that Ly6Chi acquired CD64 expression and converted into Ym1 and Relm-α-expressing CD11bhi Mφ, while these markers were expressed at significantly low levels in Il4ra−/loxlyz2Cre mice. CD11bhi Mφ accumulated at the cost of resident CD11blo KCs, which could suggest that S. mansoni infection causes KC disappearance resulting in recruitment of monocytes to the liver. Indeed, ablation of resident KCs in CD169-DTR mice resulted in the accumulation of a CD11bhi Mφ population similar to the one observed after S. mansoni infection. Thus, our findings indicate that S. mansoni infection is associated with ablation of resident KCs which could in turn result in the accumulation of M(IL-4) in the liver to control granulomatous inflammation. [less ▲]

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See detailHelminth-induced IL-4 expands bystander memory CD8+ T cells for early control of viral infection
Rolot, Marion; Dougall, Annette; Chetty, Alisha et al

Conference (2018, August)

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8+ T cells (TVM) are non-conventional T cells displaying memory ... [more ▼]

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8+ T cells (TVM) are non-conventional T cells displaying memory properties that can be generated through responsiveness to interleukin (IL)-4. However, it is not clear if helminth-induced type 2 immunity functionally affects the TVM compartment. Here, we show that helminths expand CD44hiCD62LhiCXCR3hiCD49dlo TVM cells through direct IL-4 signaling in CD8+ T cells. Importantly, helminth-mediated conditioning of TVM cells provided enhanced control of acute respiratory infection with the murid gammaherpesvirus 4 (MuHV-4). This enhanced control of MuHV-4 infection could further be explained by an increase in antigen-specific CD8+ T cell effector responses in the lung and was directly dependent on IL-4 signaling. These results demonstrate that IL-4 during helminth infection can non-specifically condition CD8+ T cells, leading to a subsequently raised antigen-specific CD8+ T cell activation that enhanced control of viral infection. [less ▲]

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See detailMaternal helminth infections and the shaping of offspring immunity.
Dewals, Benjamin G ULiege; Layland, Laura E.; Prazeres da Costa, Clarissa et al

in Parasite Immunology (2018)

Helminth infections leave a long lasting immunological footprint on their hosts. Clinical studies have provided first evidence that maternal helminth infections can result in an altered immune profile in ... [more ▼]

Helminth infections leave a long lasting immunological footprint on their hosts. Clinical studies have provided first evidence that maternal helminth infections can result in an altered immune profile in their offspring which can potentially shape how they respond to conditions throughout life. This can relate to changes in offspring induction of immune responses against other diseases. However, if these changes result in actual changes in offspring ability to control disease is unclear. Our understanding of which immune mechanisms are altered and how they are changed is limited. In this review, we highlight what we know from human and mouse studies about this important context of helminth exposure. Moreover, we discuss how mechanisms such as antibody transfer, antigen exposure, maternal cell uptake, chimerism and epigenetics are all likely to be functional contributors to the striking changes that are seen in offspring born or nursed by helminth exposed mothers. This article is protected by copyright. All rights reserved. [less ▲]

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See detailHelminth-induced IL-4 expands bystander memory CD8(+) T cells for early control of viral infection.
Rolot, Marion ULiege; Dougall, Annette M.; Chetty, Alisha et al

in Nature Communications (2018), 9(1), 4516

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8(+) T cells (TVM) are non-conventional T cells displaying ... [more ▼]

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8(+) T cells (TVM) are non-conventional T cells displaying memory properties that can be generated through responsiveness to interleukin (IL)-4. However, it is not clear if helminth-induced type 2 immunity functionally affects the TVM compartment. Here, we show that helminths expand CD44(hi)CD62L(hi)CXCR3(hi)CD49d(lo) TVM cells through direct IL-4 signaling in CD8(+) T cells. Importantly, helminth-mediated conditioning of TVM cells provided enhanced control of acute respiratory infection with the murid gammaherpesvirus 4 (MuHV-4). This enhanced control of MuHV-4 infection could further be explained by an increase in antigen-specific CD8(+) T cell effector responses in the lung and was directly dependent on IL-4 signaling. These results demonstrate that IL-4 during helminth infection can non-specifically condition CD8(+) T cells, leading to a subsequently raised antigen-specific CD8(+) T cell activation that enhances control of viral infection. [less ▲]

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See detailMacrophage Activation and Functions during Helminth Infection: Recent Advances from the Laboratory Mouse.
Rolot, Marion ULiege; Dewals, Benjamin G ULiege

in Journal of Immunology Research (2018), 2018

Macrophages are highly plastic innate immune cells that adopt an important diversity of phenotypes in response to environmental cues. Helminth infections induce strong type 2 cell-mediated immune ... [more ▼]

Macrophages are highly plastic innate immune cells that adopt an important diversity of phenotypes in response to environmental cues. Helminth infections induce strong type 2 cell-mediated immune responses, characterized among other things by production of high levels of interleukin- (IL-) 4 and IL-13. Alternative activation of macrophages by IL-4 in vitro was described as an opposite phenotype of classically activated macrophages, but the in vivo reality is much more complex. Their exact activation state as well as the role of these cells and associated molecules in type 2 immune responses remains to be fully understood. We can take advantage of a variety of helminth models available, each of which have their own feature including life cycle, site of infection, or pathological mechanisms influencing macrophage biology. Here, we reviewed the recent advances from the laboratory mouse about macrophage origin, polarization, activation, and effector functions during parasitic helminth infection. [less ▲]

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See detailSeroprevalence of malignant catarrhal fever virus in captive wildebeest (Connochaetes sp.) in France.
Ortiz, Katia; Javaux, Justine ULiege; Simon, Marie et al

in Transboundary and Emerging Diseases (2018)

Alcelaphine herpesvirus 1 (AlHV-1) is a gammaherpesvirus carried asymptomatically by wildebeests (Connochaetes sp.) in sub-Saharan Africa. Although asymptomatic in wildebeest, AlHV-1 infection in a number ... [more ▼]

Alcelaphine herpesvirus 1 (AlHV-1) is a gammaherpesvirus carried asymptomatically by wildebeests (Connochaetes sp.) in sub-Saharan Africa. Although asymptomatic in wildebeest, AlHV-1 infection in a number of other ruminant species causes a severe and fatal lymphoproliferative disease named wildebeest-derived malignant catarrhal fever (WD-MCF). Several endangered species of captive ruminants are highly susceptible to developing WD-MCF if infected by AlHV-1, which is a critical concern in zoos, game reserves and wildlife parks where wildebeests are also kept in captivity. Here, we investigated the seroprevalence of AlHV-1 in 52 captive wildebeests randomly sampled from five different zoos in France. We found 46% (24/52) seropositive animals and detected AlHV-1 DNA in one of them, demonstrating that AlHV-1 infection is present in captive wildebeests in France. In an interesting manner, the repartition of seropositive wildebeests was not homogenous between zoos with 100% (20/20) of seronegative animals in three parks. These results further highlight the importance of considering WD-MCF as a threat for clinically susceptible species and encourage for testing AlHV-1 infection in captive wildebeests as a management control strategy. [less ▲]

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