Background In December, 2019, a novel zoonotic severe acute respiratory syndrome-related coronavirus emerged in China. The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) became pandemic within weeks and the number of human infections and severe cases is increasing. We aimed to investigate the susceptibilty of potential animal hosts and the risk of anthropozoonotic spill-over infections. MethodsWe intranasally inoculated nine fruit bats (Rousettus aegyptiacus), ferrets (Mustela putorius), pigs (Sus scrofa domesticus), and 17 chickens (Gallus gallus domesticus) with 10⁵ TCID 50 of a SARS-CoV-2 isolate per animal. Direct contact animals (n=3) were included 24 h after inoculation to test viral transmission. Animals were monitored for clinical signs and for virus shedding by nucleic acid extraction from nasal washes and rectal swabs (ferrets), oral swabs and pooled faeces samples (fruit bats), nasal and rectal swabs (pigs), or oropharyngeal and cloacal swabs (chickens) on days 2, 4, 8, 12, 16, and 21 after infection by quantitative RT-PCR (RT-qPCR). On days 4, 8, and 12, two inoculated animals (or three in the case of chickens) of each species were euthanised, and all remaining animals, including the contacts, were euthanised at day 21. All animals were subjected to autopsy and various tissues were collected for virus detection by RT-qPCR, histopathology immunohistochemistry, and in situ hybridisation. Presence of SARS-CoV-2 reactive antibodies was tested by indirect immunofluorescence assay and virus neutralisation test in samples collected before inoculation and at autopsy.Findings Pigs and chickens were not susceptible to SARS-CoV-2. All swabs, organ samples, and contact animals were negative for viral RNA, and none of the pigs or chickens seroconverted. Seven (78%) of nine fruit bats had a transient infection, with virus detectable by RT-qPCR, immunohistochemistry, and in situ hybridisation in the nasal cavity, associated with rhinitis. Viral RNA was also identified in the trachea, lung, and lung-associated lymphatic tissue in two animals euthanised at day 4. One of three contact bats became infected. More efficient virus replication but no clinical signs were observed in ferrets, with transmission to all three direct contact animals. Mild rhinitis was associated with viral antigen detection in the respiratory and olfactory epithelium. Prominent viral RNA loads of 0-10⁴ viral genome copies per mL were detected in the upper respiratory tract of fruit bats and ferrets, and both species developed SARS-CoV-2-reactive antibodies reaching neutralising titres of up to 1/1024 after 21 days.Interpretation Pigs and chickens could not be infected intranasally by SARS-CoV-2, whereas fruit bats showed characteristics of a reservoir host. Virus replication in ferrets resembled a subclinical human infection with efficient spread. Ferrets might serve as a useful model for further studies-eg, testing vaccines or antivirals.Funding German Federal Ministry of Food and Agriculture.

In 2011, an unidentified disease in cattle was reported in Germany and the Netherlands. Clinical signs included fever, decreased milk production, and diarrhea. Metagenomic analysis identified a novel orthobunyavirus, which subsequently was isolated from blood of affected animals. Surveillance was initiated to test malformed newborn animals in the affected region.

Between 2011 and 2013, three breeders of variegated squirrels (Sciurus variegatoides) had encephalitis with similar clinical signs and died 2 to 4 months after onset of the clinical symptoms. With the use of a metagenomic approach that incorporated next-generation sequencing and real-time reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR), the presence of a previously unknown bornavirus was detected in a contact squirrel and in brain samples from the three patients. Phylogenetic analyses showed that this virus, tentatively named variegated squirrel 1 bornavirus (VSBV-1), forms a lineage separate from that of the known bornavirus species. (Funded by the Federal Ministry of Food and Agriculture [Germany] and others.).

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The two-component system SaeRS consisting of the histidin kinase SaeS and the response regulator SaeR is known to act on virulence gene expression in Staphylococcus aureus. In order to get a more comprehensive picture on SaeR-regulated genes, we studied the contribution of the two-component system on global gene expression by using both the proteomic and transcriptomic approach. Altogether, a loss of SaeRS resulted in a decreased amount of at least 17 extracellular proteins and two cell surface-associated proteins, among them several important virulence factors such as HlgA, HlgB, HlgC, LukF, and LukM. SaeRS activates the expression of these genes at the transcriptional level. The amount of the five proteins Aur, SspA, SsaA, Plc, and GlpQ was negatively influenced by SaeRS. However, the transcription of the corresponding genes was not affected by the two-component system. SaeRS had also no measurable influence on the transcription of the regulatory genes agr, sarA, arlRS, and sigB that contribute to the regulation of SaeRS-dependent virulence factors identified in this investigation. Our results clearly show that SaeRS is strongly involved in the tight temporal control of virulence factor expression in S. aureus. Its precise role within the regulatory network remains to be determined.Staphylococcus aureus is a gram-positive bacterium that colonizes the anterior nares of at least one-third of the human population but also causes a variety of infections ranging from superficial lesions, such as wound infections and abscesses, to severe systemic infections such as bacteremia, endocarditis, pneumonia, and osteomyelitis. The pathogenicity of this organism largely depends on the successful adaptation to the human host and the environmentally coordinated expression of virulence factors. The expression of virulence factors in S. aureus is regulated during the growth cycle by a network of interacting regulators (for a review, see reference 41). The best-characterized virulence-associated regulons thus far are the agr regulon (accessory gene regulator), the SarA regulon (staphylococcal accessory regulator), the B regulon (alternative sigma factor), the Rot regulon (regulator of toxins), and the ArlRS regulon (autolysis-regulated locus) (7,15,20,37,47,60,61).The sae locus was first described by Giraudo et al. (27) following the characterization of a Tn551 insertional mutant of S. aureus RC161. sae is a regulatory locus that consists of four open reading frames, two of them encode the response regulator and the sensor kinase, respectively (23). Two additional open reading frames coding for hypothetical proteins are probably important for the functionality of the sae operon (42, 56).

To establish a new lineage in the human population, avian influenza A viruses (AIV) must overcome the intracellular restriction factor MxA. Partial escape from MxA restriction can be achieved when the viral nucleoprotein (NP) acquires the critical human-adaptive amino acid residues 100I/V, 283P, and 313Y. Here, we show that introduction of these three residues into the NP of an avian H5N1 virus renders it genetically unstable, resulting in viruses harboring additional single mutations, including G16D. These substitutions restored genetic stability yet again yielded viruses with varying degrees of attenuation in mammalian and avian cells. Additionally, most of the mutant viruses lost the capacity to escape MxA restriction, with the exception of the G16D virus. We show that MxA escape is linked to attenuation by demonstrating that the three substitutions promoting MxA escape disturbed intracellular trafficking of incoming viral ribonucleoprotein complexes (vRNPs), thereby resulting in impaired nuclear import, and that the additional acquired mutations only partially compensate for this import block. We conclude that for adaptation to the human host, AIV must not only overcome MxA restriction but also an associated block in nuclear vRNP import. This inherent difficulty may partially explain the frequent failure of AIV to become pandemic.

We describe the first known relatives of rubella virus ( Matonaviridae : Rubivirus ) 1 in Africa and Europe. Ruhugu virus, the closest relative of rubella virus, was found in apparently healthy cyclops leaf-nosed bats ( Hipposideros cyclops ) in Uganda. Rustrela virus, outgroup to the rubella/ruhugu clade of viruses, was found in acutely encephalitic placental and marsupial animals at a zoo in Germany and in wild yellow-necked field mice ( Apodemus flavicollis ) at and near the zoo. Ruhugu and rustrela viruses share an identical genomic architecture with rubella virus 2 , 3 . Amino acid sequences of rubella, ruhugu, and rustrela viruses are moderately to highly conserved within 4 putative B-cell epitopes in the fusion (EI) protein and, in the case of rubella and ruhugu viruses, within two putative T-cell epitopes in the capsid protein 4 – 6 . Modeling of E1 homotrimers in the post-fusion state predicts similar host-cell membrane fusion capacity for ruhugu and rubella viruses 5 . Together, these findings suggest show that some members of the Matonaviridae can cross wide host species barriers and that rubella virus likely had a zoonotic origin. Our findings raise concerns about future zoonotic transmission of rubella-like viruses but open doors for heretofore impossible comparative studies and novel animal models of rubella and congenital rubella syndrome.