Concurrent infection of Bluetongue and Peste-des-petits-ruminants virus in small ruminants in Haryana State of India

Maan, Sushila; Kumar, Aman; Gupta, Akhil Kumar; Dalal, Anita; Chaudhary, Deepika; Gupta, Tarun Kumar; Bansal, Nitish; Kumar, Vinjay; Batra, Kanisht; Sindhu, Neelesh; Kumar, Ankit; Mahajan, N. K.; Maan, Narender S.; Mertens, Peter

doi:10.1111/tbed.12610

Cited by 15 publications

(8 citation statements)

References 24 publications

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“…However, PPRV is known to have an immunosuppressive effect [32], and so perhaps the co-infection of BTV and PPRV could have led to clinical bluetongue disease? PPRV and BTV co-infection has previously been reported in India [57,58]. In 2016, one year after this study, Kgotlele et al [59] investigated an outbreak of respiratory disease in Loliondo and using a multiplex assay found co-infections of PPRV with Mycoplasma capricolum subsp.…”

Section: Discussionmentioning

confidence: 80%

Characterisation of Peste Des Petits Ruminants Disease in Pastoralist Flocks in Ngorongoro District of Northern Tanzania and Bluetongue Virus Co-Infection

Jones

Mahapatra

Chubwa

et al. 2020

Viruses

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Peste des petits ruminants (PPR) disease was first confirmed in Tanzania in 2008 in sheep and goats in Ngorongoro District, northern Tanzania, and is now endemic in this area. This study aimed to characterise PPR disease in pastoralist small ruminant flocks in Ngorongoro District. During June 2015, 33 PPR-like disease reports were investigated in different parts of the district, using semi-structured interviews, clinical examinations, PPR virus rapid detection test (PPRV-RDT), and laboratory analysis. Ten flocks were confirmed as PPRV infected by PPRV-RDT and/or real-time reverse transcription-polymerase chain reaction (RT-qPCR), and two flocks were co-infected with bluetongue virus (BTV), confirmed by RT-qPCR. Phylogenetic analysis of six partial N gene sequences showed that the PPR viruses clustered with recent lineage III Tanzanian viruses, and grouped with Ugandan, Kenyan and Democratic Republic of Congo isolates. No PPR-like disease was reported in wildlife. There was considerable variation in clinical syndromes between flocks: some showed a full range of PPR signs, while others were predominantly respiratory, diarrhoea, or oro-nasal syndromes, which were associated with different local disease names (olodua—a term for rinderpest, olkipiei—lung disease, oloirobi—fever, enkorotik—diarrhoea). BTV co-infection was associated with severe oro-nasal lesions. This clinical variability makes the field diagnosis of PPR challenging, highlighting the importance of access to pen-side antigen tests and multiplex assays to support improved surveillance and targeting of control activities for PPR eradication.

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Section: Discussionmentioning

confidence: 80%

Characterisation of Peste Des Petits Ruminants Disease in Pastoralist Flocks in Ngorongoro District of Northern Tanzania and Bluetongue Virus Co-Infection

Jones

Mahapatra

Chubwa

et al. 2020

Viruses

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“…In the MENA region, perhaps due to vaccination programs, the morbidity and mortality rates do not reach these levels. There are, however, often problems with co-morbidities, perhaps due to the immune compromise by the PPR virus (Maan et al, 2017).…”

Section: Surveillance For Infectionmentioning

confidence: 99%

Assessment of Peste des Petits Ruminants (PPR) in the Middle East and North Africa Region

Hailat¹

2018

PVJ

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A regional workshop, sponsored by UN Development Program to address the problem of peste des petits ruminants (PPR) in the Middle East (Jordan and Palestine) and North African (Algeria and Egypt), (MENA) region, was held at the Jordan University of Science and Technology in February 2017. Thirty-two key scientists from universities and governments in 4 countries (Jordan, Palestine, Egypt and Algeria) gathered to present and discuss various aspects of PPR. Additionally, several farmers from the Mafraq area of Jordan participated to learn and inform. Using an interactive framework, attendees shared perspectives and gained valuable information on control of this transboundary animal disease problem. The group created a list of key issues for addressing this serious problem, including: education of farmers about clinicpathologic signs of disease for immediate reporting (passive surveillance); increasing emphasis on disease reporting (passive surveillance) as opposed to active surveillance (serologic testing); importance of sequencing isolates for variation and lineage testing; establishment of OIE reference laboratory within or close to MENA region.

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“…Notably, PPRV infection often causes foetal mummification, abortions late in pregnancy, or birth of dead or weak lambs that die within a few days [8,9]. PPRV has spread to more than 70 countries in Africa, the Near and Middle East, and Asia and is currently threatening more than 1.7 billion sheep and goats [10], causing significant economic losses [5,11]. Disease control is mostly achieved through clinical or laboratorybased diagnosis coupled with vaccination and/or slaughter.…”

Section: Introductionmentioning

confidence: 99%

Autophagy induction by the pathogen receptor NECTIN4 and sustained autophagy contribute to peste des petits ruminants virus infectivity

et al. 2019

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Macroautophagy/autophagy is an essential cellular response in the fight against intracellular pathogens. Although some viruses can escape from or utilize autophagy to ensure their own replication, the responses of autophagy pathways to viral invasion remain poorly documented. Here, we show that peste des petits ruminants virus (PPRV) infection induces successive autophagic signalling in host cells via distinct and uncoupled molecular pathways. Immediately upon invasion, PPRV induced a first transient wave of autophagy via a mechanism involving the cellular pathogen receptor NECTIN4 and an AKT-MTOR-dependent pathway. Autophagic detection showed that early PPRV infection not only increased the amounts of autophagosomes and LC3-II but also downregulated the phosphorylation of AKT-MTOR. Subsequently, we found that the binding of viral protein H to NECTIN4 ultimately induced a wave of autophagy and inactivated the AKT-MTOR pathway, which is a critical step for the control of infection. Soon after infection, new autophagic signalling was initiated that required viral replication and protein expression. Interestingly, expression of IRGM and HSPA1A was significantly upregulated following PPRV replication. Strikingly, knockdown of IRGM and HSPA1A expression using small interfering RNAs impaired the PPRV-induced second autophagic wave and viral particle production. Moreover, IRGM-interacting PPRV-C and HSPA1A-interacting PPRV-N expression was sufficient to induce autophagy through an IRGM-HSPA1A-dependent pathway. Importantly, syncytia formation could facilitate sustained autophagy and the replication of PPRV. Overall, our work reveals distinct molecular pathways underlying the induction of self-beneficial sustained autophagy by attenuated PPRV, which will contribute to improving the use of vaccines for therapy.

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Concurrent infection of Bluetongue and Peste-des-petits-ruminants virus in small ruminants in Haryana State of India

Cited by 15 publications

References 24 publications

Characterisation of Peste Des Petits Ruminants Disease in Pastoralist Flocks in Ngorongoro District of Northern Tanzania and Bluetongue Virus Co-Infection

Characterisation of Peste Des Petits Ruminants Disease in Pastoralist Flocks in Ngorongoro District of Northern Tanzania and Bluetongue Virus Co-Infection

Assessment of Peste des Petits Ruminants (PPR) in the Middle East and North Africa Region

Autophagy induction by the pathogen receptor NECTIN4 and sustained autophagy contribute to peste des petits ruminants virus infectivity

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