Erysipelothrix amsterdamensis sp. nov., associated with mortalities among endangered seabirds.

Infectious diseases threaten endangered species, particularly in small isolated populations. Seabird populations on the remote Amsterdam Island in the Indian Ocean have been in decline for the past three decades, with avian cholera caused by Pasteurella multocida proposed as the primary driver. However, Erysipelothrix species have also been sporadically detected from albatrosses on Amsterdam Island and may be contributing to some of the observed mortality. In this study, we genomically characterized 16 Erysipelothrix species isolates obtained from three Indian yellow-nosed albatross (Thalassarche carteri) chick carcasses in 2019. Histological analyses suggest that they died of bacterial septicaemia. Two isolates were sequenced using both Illumina short-read and MinION long-read approaches, which - following hybrid assembly - resulted in closed circular genomes. Mapping of Illumina reads from the remaining isolates to one of these new reference genomes revealed that all 16 isolates were closely related, with a maximum of 13 nucleotide differences distinguishing any pair of isolates. The nucleotide diversity of isolates obtained from the same or different carcasses was similar, suggesting all three chicks were likely infected from a common source. These genomes were compared with a global collection of genomes from Erysipelothrix rhusiopathiae and other species from the same genus. The isolates from albatrosses were phylogenetically distinct, sharing a most recent common ancestor with E. rhusiopathiae. Based on phylogenomic analysis and standard thresholds for average nucleotide identity and digital DNA-DNA hybridization, these isolates represent a novel Erysipelothrix species, for which we propose the name Erysipelothrix amsterdamensis sp. nov. The type strain is A18Y020dT (=CIP 112216T=DSM 115297T). The implications of this bacterium for albatross conservation will require further study.

Backyard zoonoses: The roles of companion animals and peri-domestic wildlife.

The spillover of human infectious diseases from animal reservoirs is now well appreciated. However, societal and climate-related changes are affecting the dynamics of such interfaces. In addition to the disruption of traditional wildlife habitats, in part because of climate change and human demographics and behavior, there is an increasing zoonotic disease risk from companion animals. This includes such factors as the awareness of animals kept as domestic pets and increasing populations of free-ranging animals in peri-domestic environments. This review presents background and commentary focusing on companion and peri-domestic animals as disease risk for humans, taking into account the human-animal interface and population dynamics between the animals themselves.

Disease ecology: When a GPS logger tells you more than a blood sample.

Long-term movement tracking revealed sublethal effects of avian influenza infection in vultures, adding an important element to our understanding of the subtleties of the feedback loop between host movement and pathogen transmission.

Temporal dynamics of antibody level against Lyme disease bacteria in roe deer: Tale of a sentinel?

Changes in the risk of exposure to infectious disease agents can be tracked through variations in antibody prevalence in vertebrate host populations. However, information on the temporal dynamics of the immune status of individuals is critical. If antibody levels persist a long time after exposure to an infectious agent, they could enable the efficient detection of the past circulation of the agent; if they persist only a short time, they could provide snap shots of recent exposure of sampled hosts. Here, we explored the temporal dynamics of seropositivity against Lyme disease agent Borrelia burgdorferi sensu lato (Bbsl) in individuals of a widespread medium-sized mammal species, the roe deer (Capreolus capreolus), in France. Using a modified commercially available immunoassay we tested 1554 blood samples obtained in two wild deer populations monitored from 2010 to 2020. Using multi-event capture-mark-recapture models, we estimated yearly population-, age-, and sex-specific rates of seroconversion and seroreversion after accounting for imperfect detection. The yearly seroconversion rates indicated a higher level of exposure in early (2010-2013) than in late years (2014-2019) to infected tick bites in both populations, without any detectable influence of sex or age. The relatively high rates of seroreversion indicated a short-term persistence of antibody levels against Bbsl in roe deer. This was confirmed by the analysis of samples collected on a set of captive individuals that were resampled several times a few weeks apart. Our findings show the potential usefulness of deer as a sentinel for tracking the risk of exposure to Lyme disease Bbsl, although further investigation on the details of the antibody response to Bbsl in this incompetent host would be useful. Our study also highlights the value of combining long-term capture-mark-recapture sampling and short-time analyses of serological data for wildlife populations exposed to infectious agents of relevance to wildlife epidemiology and human health.

Comparative Aerosol and Surface Stability of SARS-CoV-2 Variants of Concern.

SARS-CoV-2 transmits principally by air; contact and fomite transmission may also occur. Variants of concern are more transmissible than ancestral SARS-CoV-2. We found indications of possible increased aerosol and surface stability for early variants of concern, but not for the Delta and Omicron variants. Stability changes are unlikely to explain increased transmissibility.

Complete Genome Sequences of Two Pasteurella multocida Isolates from Seabirds.

Pasteurella multocida is one of the major causes of mass mortalities in wild birds. Here, we report the complete genome sequences of two P. multocida isolates from wild populations of two endangered seabird species, the Indian yellow-nosed albatrosses (Thalassarche carteri) and the northern rockhopper penguins (Eudyptes moseleyi).

Climate change in the Arctic: Testing the poleward expansion of ticks and tick-borne diseases.

Climate change is most strongly felt in the polar regions of the world, with significant impacts on the species that live there. The arrival of parasites and pathogens from more temperate areas may become a significant problem for these populations, but current observations of parasite presence often lack a historical reference of prior absence. Observations in the high Arctic of the seabird tick Ixodes uriae suggested that this species expanded poleward in the last two decades in relation to climate change. As this tick can have a direct impact on the breeding success of its seabird hosts and vectors several pathogens, including Lyme disease spirochaetes, understanding its invasion dynamics is essential for predicting its impact on polar seabird populations. Here, we use population genetic data and host serology to test the hypothesis that I. uriae recently expanded into Svalbard. Both black-legged kittiwakes (Rissa tridactyla) and thick-billed murres (Uria lomvia) were sampled for ticks and blood in Kongsfjorden, Spitsbergen. Ticks were genotyped using microsatellite markers and population genetic analyses were performed using data from 14 reference populations from across the tick's northern distribution. In contrast to predictions, the Spitsbergen population showed high genetic diversity and significant differentiation from reference populations, suggesting long-term isolation. Host serology also demonstrated a high exposure rate to Lyme disease spirochaetes (Bbsl). Targeted PCR and sequencing confirmed the presence of Borrelia garinii in a Spitsbergen tick, demonstrating the presence of Lyme disease bacteria in the high Arctic for the first time. Taken together, results contradict the notion that I. uriae has recently expanded into the high Arctic. Rather, this tick has likely been present for some time, maintaining relatively high population sizes and an endemic transmission cycle of Bbsl. Close future observations of population infestation/infection rates will now be necessary to relate epidemiological changes to ongoing climate modifications.

Comparative aerosol and surface stability of SARS-CoV-2 Variants of Concern.

SARS-CoV-2 is transmitted principally via air; contact and fomite transmission may also occur. Variants-of-concern (VOCs) are more transmissible than ancestral SARS-CoV-2. We find that early VOCs show greater aerosol and surface stability than the early WA1 strain, but Delta and Omicron do not. Stability changes do not explain increased transmissibility.

Ecology, evolution and spillover of coronaviruses from bats.

In the past two decades, three coronaviruses with ancestral origins in bats have emerged and caused widespread outbreaks in humans, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since the first SARS epidemic in 2002-2003, the appreciation of bats as key hosts of zoonotic coronaviruses has advanced rapidly. More than 4,000 coronavirus sequences from 14 bat families have been identified, yet the true diversity of bat coronaviruses is probably much greater. Given that bats are the likely evolutionary source for several human coronaviruses, including strains that cause mild upper respiratory tract disease, their role in historic and future pandemics requires ongoing investigation. We review and integrate information on bat-coronavirus interactions at the molecular, tissue, host and population levels. We identify critical gaps in knowledge of bat coronaviruses, which relate to spillover and pandemic risk, including the pathways to zoonotic spillover, the infection dynamics within bat reservoir hosts, the role of prior adaptation in intermediate hosts for zoonotic transmission and the viral genotypes or traits that predict zoonotic capacity and pandemic potential. Filling these knowledge gaps may help prevent the next pandemic.

Drivers and Distribution of Henipavirus-Induced Syncytia: What Do We Know?

Syncytium formation, i.e., cell-cell fusion resulting in the formation of multinucleated cells, is a hallmark of infection by paramyxoviruses and other pathogenic viruses. This natural mechanism has historically been a diagnostic marker for paramyxovirus infection in vivo and is now widely used for the study of virus-induced membrane fusion in vitro. However, the role of syncytium formation in within-host dissemination and pathogenicity of viruses remains poorly understood. The diversity of henipaviruses and their wide host range and tissue tropism make them particularly appropriate models with which to characterize the drivers of syncytium formation and the implications for virus fitness and pathogenicity. Based on the henipavirus literature, we summarized current knowledge on the mechanisms driving syncytium formation, mostly acquired from in vitro studies, and on the in vivo distribution of syncytia. While these data suggest that syncytium formation widely occurs across henipaviruses, hosts, and tissues, we identified important data gaps that undermined our understanding of the role of syncytium formation in virus pathogenesis. Based on these observations, we propose solutions of varying complexity to fill these data gaps, from better practices in data archiving and publication for in vivo studies, to experimental approaches in vitro.

Heat-Treated Virus Inactivation Rate Depends Strongly on Treatment Procedure: Illustration with SARS-CoV-2.

Decontamination helps limit environmental transmission of infectious agents. It is required for the safe reuse of contaminated medical, laboratory, and personal protective equipment, and for the safe handling of biological samples. Heat treatment is a common decontamination method, notably used for viruses. We show that for liquid specimens (here, solution of SARS-CoV-2 in cell culture medium), the virus inactivation rate under heat treatment at 70°C can vary by almost two orders of magnitude depending on the treatment procedure, from a half-life of 0.86 min (95% credible interval [CI] 0.09, 1.77) in closed vials in a heat block to 37.04 min (95% CI 12.64, 869.82) in uncovered plates in a dry oven. These findings suggest a critical role of evaporation in virus inactivation via dry heat. Placing samples in open or uncovered containers may dramatically reduce the speed and efficacy of heat treatment for virus inactivation. Given these findings, we reviewed the literature on temperature-dependent coronavirus stability and found that specimen container types, along with whether they are closed, covered, or uncovered, are rarely reported in the scientific literature. Heat-treatment procedures must be fully specified when reporting experimental studies to facilitate result interpretation and reproducibility, and must be carefully considered when developing decontamination guidelines. IMPORTANCE Heat is a powerful weapon against most infectious agents. It is widely used for decontamination of medical, laboratory, and personal protective equipment, and for biological samples. There are many methods of heat treatment, and methodological details can affect speed and efficacy of decontamination. We applied four different heat-treatment procedures to liquid specimens containing SARS-CoV-2. Our results show that the container used to store specimens during decontamination can substantially affect inactivation rate; for a given initial level of contamination, decontamination time can vary from a few minutes in closed vials to several hours in uncovered plates. Reviewing the literature, we found that container choices and heat treatment methods are only rarely reported explicitly in methods sections. Our study shows that careful consideration of heat-treatment procedure-in particular the choice of specimen container and whether it is covered-can make results more consistent across studies, improve decontamination practice, and provide insight into the mechanisms of virus inactivation.

Headless Henipaviral Receptor Binding Glycoproteins Reveal Fusion Modulation by the Head/Stalk Interface and Post-receptor Binding Contributions of the Head Domain.

Cedar virus (CedV) is a nonpathogenic member of the Henipavirus (HNV) genus of emerging viruses, which includes the deadly Nipah (NiV) and Hendra (HeV) viruses. CedV forms syncytia, a hallmark of henipaviral and paramyxoviral infections and pathogenicity. However, the intrinsic fusogenic capacity of CedV relative to NiV or HeV remains unquantified. HNV entry is mediated by concerted interactions between the attachment (G) and fusion (F) glycoproteins. Upon receptor binding by the HNV G head domain, a fusion-activating G stalk region is exposed and triggers F to undergo a conformational cascade that leads to viral entry or cell-cell fusion. Here, we demonstrate quantitatively that CedV is inherently significantly less fusogenic than NiV at equivalent G and F cell surface expression levels. We then generated and tested six headless CedV G mutants of distinct C-terminal stalk lengths, surprisingly revealing highly hyperfusogenic cell-cell fusion phenotypes 3- to 4-fold greater than wild-type CedV levels. Additionally, similarly to NiV, a headless HeV G mutant yielded a less pronounced hyperfusogenic phenotype compared to wild-type HeV. Further, coimmunoprecipitation and cell-cell fusion assays revealed heterotypic NiV/CedV functional G/F bidentate interactions, as well as evidence of HNV G head domain involvement beyond receptor binding or G stalk exposure. All evidence points to the G head/stalk junction being key to modulating HNV fusogenicity, supporting the notion that head domains play several distinct and central roles in modulating stalk domain fusion promotion. Further, this study exemplifies how CedV may help elucidate important mechanistic underpinnings of HNV entry and pathogenicity. IMPORTANCE The Henipavirus genus in the Paramyxoviridae family includes the zoonotic Nipah (NiV) and Hendra (HeV) viruses. NiV and HeV infections often cause fatal encephalitis and pneumonia, but no vaccines or therapeutics are currently approved for human use. Upon viral entry, Henipavirus infections yield the formation of multinucleated cells (syncytia). Viral entry and cell-cell fusion are mediated by the attachment (G) and fusion (F) glycoproteins. Cedar virus (CedV), a nonpathogenic henipavirus, may be a useful tool to gain knowledge on henipaviral pathogenicity. Here, using homotypic and heterotypic full-length and headless CedV, NiV, and HeV G/F combinations, we discovered that CedV G/F are significantly less fusogenic than NiV or HeV G/F, and that the G head/stalk junction is key to modulating cell-cell fusion, refining the mechanism of henipaviral membrane fusion events. Our study exemplifies how CedV may be a useful tool to elucidate broader mechanistic understanding for the important henipaviruses.

Mechanistic theory predicts the effects of temperature and humidity on inactivation of SARS-CoV-2 and other enveloped viruses.

Ambient temperature and humidity strongly affect inactivation rates of enveloped viruses, but a mechanistic, quantitative theory of these effects has been elusive. We measure the stability of SARS-CoV-2 on an inert surface at nine temperature and humidity conditions and develop a mechanistic model to explain and predict how temperature and humidity alter virus inactivation. We find SARS-CoV-2 survives longest at low temperatures and extreme relative humidities (RH); median estimated virus half-life is >24 hr at 10°C and 40% RH, but ∼1.5 hr at 27°C and 65% RH. Our mechanistic model uses fundamental chemistry to explain why inactivation rate increases with increased temperature and shows a U-shaped dependence on RH. The model accurately predicts existing measurements of five different human coronaviruses, suggesting that shared mechanisms may affect stability for many viruses. The results indicate scenarios of high transmission risk, point to mitigation strategies, and advance the mechanistic study of virus transmission.

SARS-CoV-2: Cross-scale Insights from Ecology and Evolution.

Ecological and evolutionary processes govern the fitness, propagation, and interactions of organisms through space and time, and viruses are no exception. While coronavirus disease 2019 (COVID-19) research has primarily emphasized virological, clinical, and epidemiological perspectives, crucial aspects of the pandemic are fundamentally ecological or evolutionary. Here, we highlight five conceptual domains of ecology and evolution - invasion, consumer-resource interactions, spatial ecology, diversity, and adaptation - that illuminate (sometimes unexpectedly) the emergence and spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We describe the applications of these concepts across levels of biological organization and spatial scales, including within individual hosts, host populations, and multispecies communities. Together, these perspectives illustrate the integrative power of ecological and evolutionary ideas and highlight the benefits of interdisciplinary thinking for understanding emerging viruses.

Risk assessment of SARS-CoV-2 in Antarctic wildlife.

The coronavirus disease 2019 (COVID-19) pandemic is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This pathogen has spread rapidly across the world, causing high numbers of deaths and significant social and economic impacts. SARS-CoV-2 is a novel coronavirus with a suggested zoonotic origin with the potential for cross-species transmission among animals. Antarctica can be considered the only continent free of SARS-CoV-2. Therefore, concerns have been expressed regarding the potential human introduction of this virus to the continent through the activities of research or tourism to minimise the effects on human health, and the potential for virus transmission to Antarctic wildlife. We assess the reverse-zoonotic transmission risk to Antarctic wildlife by considering the available information on host susceptibility, dynamics of the infection in humans, and contact interactions between humans and Antarctic wildlife. The environmental conditions in Antarctica seem to be favourable for the virus stability. Indoor spaces such as those at research stations, research vessels or tourist cruise ships could allow for more transmission among humans and depending on their movements between different locations the virus could be spread across the continent. Among Antarctic wildlife previous in silico analyses suggested that cetaceans are at greater risk of infection whereas seals and birds appear to be at a low infection risk. However, caution needed until further research is carried out and consequently, the precautionary principle should be applied. Field researchers handling animals are identified as the human group posing the highest risk of transmission to animals while tourists and other personnel pose a significant risk only when in close proximity (< 5 m) to Antarctic fauna. We highlight measures to reduce the risk as well as identify of knowledge gaps related to this issue.

Heat-treated virus inactivation rate depends strongly on treatment procedure: illustration with SARS-CoV-2.

Decontamination helps limit environmental transmission of infectious agents. It is required for the safe re-use of contaminated medical, laboratory and personal protective equipment, and for the safe handling of biological samples. Heat treatment is a common decontamination method, notably used for viruses. We show that for liquid specimens (here, solution of SARS-CoV-2 in cell culture medium), virus inactivation rate under heat treatment at 70°C can vary by almost two orders of magnitude depending on the treatment procedure, from a half-life of 0.86 min (95% credible interval: [0.09, 1.77]) in closed vials in a heat block to 37.00 min ([12.65, 869.82]) in uncovered plates in a dry oven. These findings suggest a critical role of evaporation in virus inactivation via dry heat. Placing samples in open or uncovered containers may dramatically reduce the speed and efficacy of heat treatment for virus inactivation. Given these findings, we reviewed the literature temperature-dependent coronavirus stability and found that specimen containers, and whether they are closed, covered, or uncovered, are rarely reported in the scientific literature. Heat-treatment procedures must be fully specified when reporting experimental studies to facilitate result interpretation and reproducibility, and must be carefully considered when developing decontamination guidelines.

Mechanistic theory predicts the effects of temperature and humidity on inactivation of SARS-CoV-2 and other enveloped viruses.

Environmental conditions affect virus inactivation rate and transmission potential. Understanding those effects is critical for anticipating and mitigating epidemic spread. Ambient temperature and humidity strongly affect the inactivation rate of enveloped viruses, but a mechanistic, quantitative theory of those effects has been elusive. We measure the stability of the enveloped respiratory virus SARS-CoV-2 on an inert surface at nine temperature and humidity conditions and develop a mechanistic model to explain and predict how temperature and humidity alter virus inactivation. We find SARS-CoV-2 survives longest at low temperatures and extreme relative humidities; median estimated virus half-life is over 24 hours at 10 °C and 40 % RH, but approximately 1.5 hours at 27 °C and 65 % RH. Our mechanistic model uses simple chemistry to explain the increase in virus inactivation rate with increased temperature and the U-shaped dependence of inactivation rate on relative humidity. The model accurately predicts quantitative measurements from existing studies of five different human coronaviruses (including SARS-CoV-2), suggesting that shared mechanisms may determine environmental stability for many enveloped viruses. Our results indicate scenarios of particular transmission risk, point to pandemic mitigation strategies, and open new frontiers in the mechanistic study of virus transmission.

Quantifying antibody kinetics and RNA detection during early-phase SARS-CoV-2 infection by time since symptom onset.

Understanding and mitigating SARS-CoV-2 transmission hinges on antibody and viral RNA data that inform exposure and shedding, but extensive variation in assays, study group demographics and laboratory protocols across published studies confounds inference of true biological patterns. Our meta-analysis leverages 3214 datapoints from 516 individuals in 21 studies to reveal that seroconversion of both IgG and IgM occurs around 12 days post-symptom onset (range 1-40), with extensive individual variation that is not significantly associated with disease severity. IgG and IgM detection probabilities increase from roughly 10% at symptom onset to 98-100% by day 22, after which IgM wanes while IgG remains reliably detectable. RNA detection probability decreases from roughly 90% to zero by day 30, and is highest in feces and lower respiratory tract samples. Our findings provide a coherent evidence base for interpreting clinical diagnostics, and for the mathematical models and serological surveys that underpin public health policies.

Impact of Annual Bacterial Epizootics on Albatross Population on a Remote Island.

The reduced species richness typical of oceanic islands provides an interesting environmental setup to examine in natura the epidemiological dynamics of infectious agents with potential implications for public health and/or conservation. On Amsterdam Island (Indian Ocean), recurrent die-offs of Indian yellow-nosed albatross (Thalassarche carteri) nestlings have been attributed to avian cholera, caused by the bacterium Pasteurella multocida. In order to help implementing efficient measures for the control of this disease, it is critical to better understand the local epidemiology of P. multocida and to examine its inter- and intra-annual infection dynamics. We evaluated the infection status of 264 yellow-nosed albatrosses over four successive breeding seasons using a real-time PCR targeting P. multocida DNA from cloacal swabs. Infection prevalence patterns revealed an intense circulation of P. multocida throughout the survey, with a steady but variable increase in infection prevalence within each breeding season. These epizootics were associated with massive nestling dies-offs, inducing very low fledging successes (≤ 20%). These results suggest important variations in the transmission dynamics of this pathogen. These findings and the developed PCR protocol have direct applications to guide future research and refine conservation plans aiming at controlling the disease.