Nipah virus dynamics in bats and implications for spillover to humans

Nipah virus (NiV) is an emerging bat-borne zoonotic virus that causes near-annual outbreaks of fatal encephalitis in South Asia-one of the most populous regions on Earth. In Bangladesh, infection occurs when people drink date-palm sap contaminated with bat excreta. Outbreaks are sporadic, and the influence of viral dynamics in bats on their temporal and spatial distribution is poorly understood. We analyzed data on host ecology, molecular epidemiology, serological dynamics, and viral genetics to characterize spatiotemporal patterns of NiV dynamics in its wildlife reservoir, bats, in Bangladesh. We found that NiV transmission occurred throughout the country and throughout the year. Model results indicated that local transmission dynamics were modulated by density-dependent transmission, acquired immunity that is lost over time, and recrudescence. Increased transmission followed multiyear periods of declining seroprevalence due to bat-population turnover and individual loss of humoral immunity. Individual bats had smaller host ranges than other species (spp.), although movement data and the discovery of a Malaysia-clade NiV strain in eastern Bangladesh suggest connectivity with bats east of Bangladesh. These data suggest that discrete multiannual local epizootics in bat populations contribute to the sporadic nature of NiV outbreaks in South Asia. At the same time, the broad spatial and temporal extent of NiV transmission, including the recent outbreak in Kerala, India, highlights the continued risk of spillover to humans wherever they may interact with pteropid bats and the importance of limiting opportunities for spillover throughout 's range. [Abstract copyright: Copyright © 2020 the Author(s). Published by PNAS.

Vaccination of koalas (Phascolarctos cinereus) against Chlamydia pecorum using synthetic peptides derived from the major outer membrane protein.

Chlamydia pecorum is a mucosal infection, which causes debilitating disease of the urinary tract, reproductive tract and ocular sites of koalas (Phascolarctos cinereus). While antibiotics are available for treatment, they are detrimental to the koalas' gastrointestinal tract microflora leaving the implementation of a vaccine as an ideal option for the long-term management of koala populations. We have previously reported on the successes of an anti-chlamydial recombinant major outer membrane protein (rMOMP) vaccine however, recombinant protein based vaccines are not ideal candidates for scale up from the research level to small-medium production level for wider usage. Peptide based vaccines are a promising area for vaccine development, because peptides are stable, cost effective and easily produced. In this current study, we assessed, for the first time, the immune responses to a synthetic peptide based anti-chlamydial vaccine in koalas. Five healthy male koalas were vaccinated with two synthetic peptides derived from C. pecorum MOMP and another five healthy male koalas were vaccinated with full length recombinant C. pecorum MOMP (genotype G). Systemic (IgG) and mucosal (IgA) antibodies were quantified and pre-vaccination levels compared to post-vaccination levels (12 and 26 weeks). MOMP-peptide vaccinated koalas produced Chlamydia-specific IgG and IgA antibodies, which were able to recognise not only the genotype used in the vaccination, but also MOMPs from several other koala C. pecorum genotypes. In addition, IgA antibodies induced at the ocular site not only recognised recombinant MOMP protein but also, whole native chlamydial elementary bodies. Interestingly, some MOMP-peptide vaccinated koalas showed a stronger and more sustained vaccine-induced mucosal IgA antibody response than observed in MOMP-protein vaccinated koalas. These results demonstrate that a synthetic MOMP peptide based vaccine is capable of inducing a Chlamydia-specific antibody response in koalas and is a promising candidate for future vaccine development

Role of Environmental Temperature on the Attack rate and Case fatality rate of Coronavirus Disease 2019 (COVID-19) Pandemic

SARS-CoV-2 is a zoonotic Betacoronavirus causing the devastating COVID-19 pandemic. More than twelve million COVID-19 cases and 500 thousand fatalities have been reported in 216 countries. Although SARS-CoV-2 originated in China, comparatively fewer people have been affected in other Asian countries than in Europe and the USA. This study examined the hypothesis that lower temperature may increase the spread of SARS-CoV-2 by comparing attack rate and case fatality rate (until 21 March 2020) to mean temperature in January–February 2020. The attack rate was highest in Luxembourg followed by Italy and Switzerland. There was a significant (p = 0.02) correlation between decreased attack rate and increased environmental temperature. The case fatality rate was highest in Italy followed by Iran and Spain. There was no significant correlation between the case fatality rate and temperature. This study indicates that lower temperature may increase SARS-CoV-2 transmission (measured as an increased attack rate), but there is no evidence that temperature affects the severity of the disease (measured as case fatality rate). However, there are clearly other factors that affect the transmission of SARS-CoV-2, and many of these may be sensitive to interventions, e.g. through increased public awareness and public health response

Prevalence and Diversity of Avian Influenza Virus Hemagglutinin Sero-Subtypes in Poultry and Wild Birds in Bangladesh

Highly pathogenic avian influenza H5 viruses have pandemic potential, cause significant economic losses and are of veterinary and public health concerns. This study aimed to investigate the distribution and diversity of hemagglutinin (HA) subtypes of avian influenza virus (AIV) in poultry and wild birds in Bangladesh. We conducted an avian influenza sero-surveillance in wild and domestic birds in wetlands of Chattogram and Sylhet in the winter seasons 2012-2014. We tested serum samples using a competitive enzyme-linked immunosorbent assay (c-ELISA), and randomly selected positive serum samples (170 of 942) were tested using hemagglutination inhibition (HI) to detect antibodies against the 16 different HA sero-subtypes. All AIV sero-subtypes except H7, H11, H14 and H15 were identified in the present study, with H5 and H9 dominating over other subtypes, regardless of the bird species. The diversity of HA sero-subtypes within groups ranged from 3 (in household chickens) to 10 (in migratory birds). The prevalence of the H5 sero-subtype was 76.3% (29/38) in nomadic ducks, 71.4% (5/7) in household chicken, 66.7% (24/36) in resident wild birds, 65.9% (27/41) in migratory birds and 61.7% (29/47) in household ducks. Moreover, the H9 sero-subtype was common in migratory birds (56%; 23/41), followed by 38.3% (18/47) in household ducks, 36.8% (14/38) in nomadic ducks, 30.6% (11/66) in resident wild birds and 28.5% (2/7) in household chickens. H1, H4 and H6 sero-subtypes were the most common sero-subtypes (80%; 8/10, 70%; 7/10 and 70%; 7/10, respectively) in migratory birds in 2012, H9 in resident wild birds (83.3%; 5/6) and H2 in nomadic ducks (73.9%; 17/23) in 2013, and the H5 sero-subtype in all types of birds (50% to 100%) in 2014. The present study demonstrates that a high diversity of HA subtypes circulated in diverse bird species in Bangladesh, and this broad range of AIV hosts may increase the probability of AIVs' reassortment and may enhance the emergence of novel AIV strains. A continued surveillance for AIV at targeted domestic-wild bird interfaces is recommended to understand the ecology and evolution of AIVs

MOMP-peptide vaccinated koalas (<i>Phascolarctos cinereus</i>) produced a systemic IgG antibody response to the peptides P1 and P2.

<p>Systemic IgG antibody response (from plasma) against two different synthetic peptides (P1 and P2) measured pre-vaccination and at 12 and 26 weeks post-vaccination. Samples were analysed by ELISA and measurments are shown as EPT. (A) MOMP-peptide vaccinated koalas (n = 5) response against P1. (B) MOMP-protein vaccinated koalas (n = 5) response against P1. (C) MOMP-peptide vaccinated koalas (n = 5) response against P2. (D) MOMP-protein vaccinated koalas (n = 5) response against P2.</p

MOMP-peptide vaccinated koalas (<i>Phascolarctos cinereus</i>) produced a systemic IgG antibody response to rMOMP proteins.

<p>Systemic IgG antibody response (from plasma) against recombinant protein from <i>Chlamydia pecorum</i> MOMP genotypes A, F and G measured pre-vaccination and at 12 and 26 weeks post-vaccination. Samples were analysed by ELISA and measurments are shown as end point titre (EPT). (A, C and E) MOMP-peptide vaccinated koalas (n = 5) response against recombinant MOMP genotypes A, F and G, respectively. (B, D and F) MOMP-protein vaccinated koalas (n = 5) response against recombinant MOMP genotypes A, F and G, respectively.</p

MOMP-peptide vaccinated koalas (<i>Phascolarctos cinereus</i>) produced a stronger mucosal IgA antibody response to whole <i>Chlamydia pecorum</i> elementary bodies than MOMP-protein vaccinated koalas (<i>Phascolarctos cinereus</i>).

<p>Mucosal IgA antibody response to heat inactivated <i>Chlamydia pecorum</i> elementary bodies from genotype G in ocular swab samples collected pre-vaccination and 12 and 26 weeks post-vaccination. Samples were analysed by ELISA and are shown as OD measured at 450nM. (A) MOMP-peptide vaccinated koalas (n = 5) response with a P value 0.0009. (B) MOMP protein-vaccinated koalas (n = 5) response with a P value 0.0299.</p

MOMP-peptide vaccinated koalas (<i>Phascolarctos cinereus</i>) produced a stronger mucosal IgA antibody response to rMOMP protein than MOMP-protein vaccinated koalas (<i>Phascolarctos cinereus</i>).

<p>Mucosal IgA antibody response to recombinant MOMP (G) and synthetic peptides (P1 and P2) in ocular swab samples collected pre-vaccination and 12 and 26 weeks post-vaccination. Samples were analysed by ELISA and are shown as optical density (OD) measured at 450nM. (A, C and E) MOMP-peptide vaccinated koalas (n = 5) response to recombinant MOMP G, peptide P1 and peptide P2, respectively. (B, D and F) MOMP-protein vaccinated koalas (n = 5) response to recombinant MOMP G, peptide P1 and peptide P2, respectively.</p

A strategy to estimate unknown viral diversity in mammals.

UnlabelledThe majority of emerging zoonoses originate in wildlife, and many are caused by viruses. However, there are no rigorous estimates of total viral diversity (here termed "virodiversity") for any wildlife species, despite the utility of this to future surveillance and control of emerging zoonoses. In this case study, we repeatedly sampled a mammalian wildlife host known to harbor emerging zoonotic pathogens (the Indian Flying Fox, Pteropus giganteus) and used PCR with degenerate viral family-level primers to discover and analyze the occurrence patterns of 55 viruses from nine viral families. We then adapted statistical techniques used to estimate biodiversity in vertebrates and plants and estimated the total viral richness of these nine families in P. giganteus to be 58 viruses. Our analyses demonstrate proof-of-concept of a strategy for estimating viral richness and provide the first statistically supported estimate of the number of undiscovered viruses in a mammalian host. We used a simple extrapolation to estimate that there are a minimum of 320,000 mammalian viruses awaiting discovery within these nine families, assuming all species harbor a similar number of viruses, with minimal turnover between host species. We estimate the cost of discovering these viruses to be ~$6.3 billion (or ~$1.4 billion for 85% of the total diversity), which if annualized over a 10-year study time frame would represent a small fraction of the cost of many pandemic zoonoses.ImportanceRecent years have seen a dramatic increase in viral discovery efforts. However, most lack rigorous systematic design, which limits our ability to understand viral diversity and its ecological drivers and reduces their value to public health intervention. Here, we present a new framework for the discovery of novel viruses in wildlife and use it to make the first-ever estimate of the number of viruses that exist in a mammalian host. As pathogens continue to emerge from wildlife, this estimate allows us to put preliminary bounds around the potential size of the total zoonotic pool and facilitates a better understanding of where best to allocate resources for the subsequent discovery of global viral diversity