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Lassa fever is a severe viral hemorrhagic fever caused by a zoonotic virus that repeatedly spills over to humans from its rodent reservoirs. It is currently not known how climate and land use changes could affect the endemic area of this virus, currently limited to parts of West Africa. By exploring the environmental data associated with virus occurrence using ecological niche modelling, we show how temperature, precipitation and the presence of pastures determine ecological suitability for virus circulation. Based on projections of climate, land use, and population changes, we find that regions in Central and East Africa will likely become suitable for Lassa virus over the next decades and estimate that the total population living in ecological conditions that are suitable for Lassa virus circulation may drastically increase by 2070. By analysing geotagged viral genomes using spatially-explicit phylogeography and simulating virus dispersal, we find that in the event of Lassa virus being introduced into a new suitable region, its spread might remain spatially limited over the first decades.

The need to estimate divergence times in evolutionary histories in the presence of various sources of substitution rate variation has stimulated a rich development of relaxed molecular clock models. Viral evolutionary studies frequently adopt an uncorrelated clock model as a generic relaxed molecular clock process, but this may impose considerable estimation bias if discrete rate variation exists among clades or lineages. For HIV-1 group M, rate variation among subtypes has been shown to result in inconsistencies in time to the most recent common ancestor estimation. Although this calls into question the adequacy of available molecular dating methods, no solution to this problem has been offered so far. Here, we investigate the use of mixed effects molecular clock models, which combine both fixed and random effects in the evolutionary rate, to estimate divergence times. Using simulation, we demonstrate that this model outperforms existing molecular clock models in a Bayesian framework for estimating time-measured phylogenies in the presence of mixed sources of rate variation, while also maintaining good performance in simpler scenarios. By analysing a comprehensive HIV-1 group M complete genome data set we confirm considerable rate variation among subtypes that is not adequately modelled by uncorrelated relaxed clock models. The mixed effects clock model can accommodate this rate variation and results in a time to the most recent common ancestor of HIV-1 group M of 1920 (1915-25), which is only slightly earlier than the uncorrelated relaxed clock estimate for the same data set. The use of complete genome data appears to have a more profound impact than the molecular clock model because it reduces the credible intervals by 50 per cent relative to similar estimates based on short envelope gene sequences.

Over the past decades, the number of arthropod-borne virus (arbovirus) outbreaks has increased worldwide. Knowledge regarding the sylvatic cycle (i.e., non-human hosts/environment) of arboviruses is limited, particularly in Africa, and the main hosts for virus maintenance are unknown. Previous studies have shown the presence of antibodies against certain arboviruses (i.e., chikungunya-, dengue-, and zika virus) in African non-human primates and bats. We hypothesize that small mammals, specifically rodents, may function as amplifying hosts in anthropogenic environments. The detection of RNA of most arboviruses is complicated by the viruses' short viremic period within their hosts. An alternative to determine arbovirus hosts is by detecting antibodies, which can persist several months. Therefore, we developed a high-throughput multiplex immunoassay to detect antibodies against 15 medically relevant arboviruses. We used this assay to assess approximately 1,300 blood samples of the multimammate mouse, Mastomys natalensis from Tanzania. In 24% of the samples, we detected antibodies against at least one of the tested arboviruses, with high seroprevalences of antibodies reacting against dengue virus serotype one (7.6%) and two (8.4%), and chikungunya virus (6%). Seroprevalence was higher in females and increased with age, which could be explained by inherent immunity and behavioral differences between sexes, and the increased chance of exposure to an arbovirus with age. We evaluated whether antibodies against multiple arboviruses co-occur more often than randomly and found that this may be true for some members of the Flaviviridae and Togaviridae. In conclusion, the development of an assay against a wide diversity of medically relevant arboviruses enabled the analysis of a large sample collection of one of the most abundant African small mammals. Our findings highlight that Mastomys natalensis is involved in the transmission cycle of multiple arboviruses and provide a solid foundation to better understand the role of this ubiquitous rodent in arbovirus outbreaks. Author summary: One of the main causes of zoonotic related human morbidity and mortality is the transmission of arthropod-borne viruses such as dengue virus, Yellow Fever virus, and chikungunya virus. These viruses cannot only infect humans but also livestock, pets, and wildlife, though our understanding of their non-human hosts remains limited. Rodents are thought to be an important host for these viruses because they can be abundant, often live near humans, and some are already known to be viral hosts. However, research has focused mostly on non-human primates, neglecting other potential wild hosts. To address this gap, we have developed a high-throughput antibody test to screen rodent blood against 15 different arboviruses. Our findings reveal that Mastomys natalensis, a common African rodent species, carries antibodies that (cross-)react against these viruses. We hypothesize that immunologically naïve juveniles may drive transmission, particularly during population outbreaks. These outbreaks coincide with environmental conditions that are favorable for mosquitoes, thus increasing the risk of spillover to humans, livestock, and wildlife. Understanding the role of rodents in arbovirus transmission dynamics is crucial for mitigating zoonotic disease risks. [ABSTRACT FROM AUTHOR]

SARS‐CoV‐2 human‐to‐animal transmission can lead to the establishment of novel reservoirs and the evolution of new variants with the potential to start new outbreaks in humans. We tested Norway rats inhabiting the sewer system of Antwerp, Belgium, for the presence of SARS‐CoV‐2 following a local COVID‐19 epidemic peak. In addition, we discuss the use and interpretation of SARS‐CoV‐2 serological tests on non‐human samples. Between November and December 2020, Norway rat oral swabs, faeces and tissues from the sewer system of Antwerp were collected to be tested by RT‐qPCR for the presence of SARS‐CoV‐2. Serum samples were screened for the presence of anti‐SARS‐CoV‐2 IgG antibodies using a Luminex microsphere immunoassay (MIA). Samples considered positive were then checked for neutralizing antibodies using a conventional viral neutralization test (cVNT). The serum of 35 rats was tested by MIA showing three potentially positive sera that were later negative by cVNT. All tissue samples of 39 rats analysed tested negative for SARS‐CoV‐2 RNA. This is the first study that evaluates SARS‐CoV‐2 infection in urban rats. We can conclude that the sample of rats analysed had never been infected with SARS‐CoV‐2. However, monitoring activities should continue due to the emergence of new variants prone to infect Muridae rodents. [ABSTRACT FROM AUTHOR]

It has been a long time since the world has experienced a pandemic with such a rapid devastating impact as the current COVID‐19 pandemic. The causative agent, severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), is unusual in that it appears capable of infecting many different mammal species. As a significant proportion of people worldwide are infected with SARS‐CoV‐2 and may spread the infection unknowingly before symptoms occur or without any symptoms ever occurring, there is a non‐negligible risk of humans spreading SARS‐CoV‐2 to wildlife, in particular to wild non‐human mammals. Because of SARS‐CoV‐2's apparent evolutionary origins in bats and reports of humans transmitting the virus to pets and zoo animals, regulations for the prevention of human‐to‐animal transmission have so far focused mostly on these animal groups. We summarise recent studies and reports that show that a wide range of distantly related mammals are likely to be susceptible to SARS‐CoV‐2, and that susceptibility or resistance to the virus is, in general, not predictable, or only predictable to some extent, from phylogenetic proximity to known susceptible or resistant hosts. In the absence of solid evidence on the susceptibility and resistance to SARS‐CoV‐2 for each of the >6500 mammal species, we argue that sanitary precautions should be taken by humans interacting with any other mammal species in the wild. Preventing human‐to‐wildlife SARS‐CoV‐2 transmission is important to protect these animals (some of which are classed as threatened) from disease, but also to avoid establishment of novel SARS‐CoV‐2 reservoirs in wild mammals. The risk of repeated re‐infection of humans from such a wildlife reservoir could severely hamper SARS‐CoV‐2 control efforts. Activities during which direct or indirect interaction with wild mammals may occur include wildlife research, conservation activities, forestry work, pest control, management of feral populations, ecological consultancy work, management of protected areas and natural environments, wildlife tourism and wildlife rehabilitation in animal shelters. During such activities, we recommend sanitary precautions, such as physical distancing, wearing face masks and gloves, and frequent decontamination, which are very similar to regulations currently imposed to prevent transmission among humans. We further recommend active surveillance of domestic and feral animals that could act as SARS‐CoV‐2 intermediate hosts between humans and wild mammals. [ABSTRACT FROM AUTHOR]

A key aim in wildlife disease ecology is to understand how host and parasite characteristics influence parasite transmission and persistence. Variation in host population density can have strong impacts on transmission and outbreaks, and theory predicts particular transmission–density patterns depending on how parasites are transmitted between individuals. Here, we present the results of a study on the dynamics of Morogoro arenavirus in a population of multimammate mice (Mastomys natalensis). This widespread African rodent, which is also the reservoir host of Lassa arenavirus in West Africa, is known for its strong seasonal density fluctuations driven by food availability.We investigated to what degree virus transmission changes with host population density and how the virus might be able to persist during periods of low host density.A seven‐year capture–mark–recapture study was conducted in Tanzania where rodents were trapped monthly and screened for the presence of antibodies against Morogoro virus. Observed seasonal seroprevalence patterns were compared with those generated by mathematical transmission models to test different hypotheses regarding the degree of density dependence and the role of chronically infected individuals.We observed that Morogoro virus seroprevalence correlates positively with host density with a lag of 1–4 months. Model results suggest that the observed seasonal seroprevalence dynamics can be best explained by a combination of vertical and horizontal transmission and that a small number of animals need to be infected chronically to ensure viral persistence.Transmission dynamics and viral persistence were best explained by the existence of both acutely and chronically infected individuals and by seasonally changing transmission rates. Due to the presence of chronically infected rodents, rodent control is unlikely to be a feasible approach for eliminating arenaviruses such as Lassa virus from Mastomys populations. [ABSTRACT FROM AUTHOR]