Temporal shifts of Bois Noir phytoplasma types infecting grapevine in South Tyrol (Northern Italy)

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Recombination, Reservoirs, and the Modular Spike: Mechanisms of Coronavirus Cross-Species Transmission

Over the past 30 years, several cross-species transmission events, as well as changes in virus tropism, have mediated significant animal and human diseases. Most notable is severe acute respiratory syndrome (SARS), a lower respiratory tract disease of humans that was first reported in late 2002 in Guangdong Province, China. The disease, which quickly spread worldwide over a period of 4 months spanning late 2002 and early 2003, infected over 8,000 individuals and killed nearly 800 before it was successfully contained by aggressive public health intervention strategies. A coronavirus (SARS-CoV) was identified as the etiological agent of SARS, and initial assessments determined that the virus crossed to human hosts from zoonotic reservoirs, including bats, Himalayan palm civets (Paguma larvata), and raccoon dogs (Nyctereutes procyonoides), sold in exotic animal markets in Guangdong Province. In this review, we discuss the molecular mechanisms that govern coronavirus cross-species transmission both in vitro and in vivo, using the emergence of SARS-CoV as a model. We pay particular attention to how changes in the Spike attachment protein, both within and outside of the receptor binding domain, mediate the emergence of coronaviruses in new host populations

Infection rates of natural psyllid populations with ‘Candidatus Phytoplasma mali’ in South Tyrol (Northern Italy)

Apple proliferation is a severe disease of apple trees spreading in many European apple growing areas. It is caused by ‘Candidatus Phytoplasma mali’ that was shown to be transmitted through infected grafting material, via natural root grafts and by sap-sucking insects. Two psyllid species, Cacopsylla picta and C. melanoneura, that are recognised as the vectors of the disease, occur in orchards of South Tyrol (Northern Italy). The aim of this study was to assess the infection rates of natural populations of these insect species with ‘Ca. P. mali’. Two additional psyllid species (C. mali and Trioza urticae), which are frequent in some apple orchards of South Tyrol, were also investigated. A total of 801 specimens from 18 orchards was analysed using a real-time PCR procedure. While no specimen of T. urticae was found to be infected with ‘Ca. P. mali’, the mean infection rate of C. melanoneura and C. mali was below 1 %. The highest infection rate was found for C. picta, with a mean value of 11 % and peaking at 33%. Based on these results, it can be concluded that C. picta plays the major role as the vector of apple proliferation in South Tyrol. Keywords: apple proliferation, Cacopsylla mali, Cacopsylla melanoneura, Cacopsylla picta, pathogen transmission, Trioza urtica

Molecular pathology of emerging coronavirus infections

Respiratory viruses can cause a wide spectrum of pulmonary diseases, ranging from mild, upper respiratory tract infections to severe and life-threatening lower respiratory tract infections, including the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Viral clearance and subsequent recovery from infection require activation of an effective host immune response; however, many immune effector cells may also cause injury to host tissues. Severe acute respiratory syndrome (SARS) coronavirus and Middle East respiratory syndrome (MERS) coronavirus cause severe infection of the lower respiratory tract, with 10% and 35% overall mortality rates, respectively; however, >50% mortality rates are seen in the aged and immunosuppressed populations. While these viruses are susceptible to interferon treatment in vitro, they both encode numerous genes that allow for successful evasion of the host immune system until after high virus titres have been achieved. In this review, we discuss the importance of the innate immune response and the development of lung pathology following human coronavirus infection

Systems approaches to coronavirus pathogenesis

Coronaviruses comprise a large group of emergent human and animal pathogens, including the highly pathogenic SARS-CoV and MERS-CoV strains that cause significant morbidity and mortality in infected individuals, especially the elderly. As emergent viruses may cause episodic outbreaks of disease over time, human samples are limited. Systems biology and genetic technologies maximize opportunities for identifying critical host and viral genetic factors that regulate susceptibility and virus-induced disease severity. These approaches provide discovery platforms that highlight and allow targeted confirmation of critical targets for prophylactics and therapeutics, especially critical in an outbreak setting. Although poorly understood, it has long been recognized that host regulation of virus-associated disease severity is multigenic. The advent of systems genetic and biology resources provide new opportunities for deconvoluting the complex genetic interactions and expression networks that regulate pathogenic or protective host response patterns following virus infection. Using SARS-CoV as a model, dynamic transcriptional network changes and disease-associated phenotypes have been identified in different genetic backgrounds, leading to the promise of population-wide discovery of the underpinnings of Coronavirus pathogenesis

Emergence of a Highly Fit SARS-CoV-2 Variant

Sarbecoviruses have emerged twice in the 21st century, causing a worldwide epidemic and pandemic. The ongoing pandemic of coronavirus disease 2019 (Covid-19), the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused unprecedented disruption of human society. Since its emergence in December 2019, SARS-CoV-2 has spread worldwide, infecting more than 70 million persons and causing more than 1.6 million deaths as of early December 2020. Previous studies have clearly shown that epidemic and pandemic RNA virus spread may select for mutations that alter RNA virus pathogenesis, virulence, transmissibility, or a combination of these, yet this process remains poorly studied among emerging coronaviruses in animals and humans

A decade after SARS: strategies for controlling emerging coronaviruses

Two novel coronaviruses have emerged in humans in the 21st century, Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrome human coronavirus (MERS-CoV), both of which cause acute respiratory distress syndrome (ARDS) and have high mortality rates. There are no clinically approved vaccines or antiviral drugs available for either of these infections; thus, a priority in the field is the development of effective therapeutic and preventive strategies that can be readily applied to new emergent strains. This review will: describe the emergence and identification of novel human coronaviruses over the last 10 years; review their key biological features, including tropism and receptor use; and summarize approaches to develop broadly effective vaccines

Severe Acute Respiratory Syndrome Coronavirus Evades Antiviral Signaling: Role of nsp1 and Rational Design of an Attenuated Strain

The severe acute respiratory syndrome (SARS) epidemic was caused by the spread of a previously unrecognized infectious agent, the SARS-associated coronavirus (SARS-CoV). Here we show that SARS-CoV could inhibit both virus- and interferon (IFN)-dependent signaling, two key steps of the antiviral response. We mapped a strong inhibitory activity to SARS-CoV nonstructural protein 1 (nsp1) and show that expression of nsp1 significantly inhibited the activation of all three virus-dependent signaling pathways. We show that expression of nsp1 significantly inhibited IFN-dependent signaling by decreasing the phosphorylation levels of STAT1 while having little effect on those of STAT2, JAK1, and TYK2. We engineered an attenuated mutant of nsp1 in SARS-CoV through reverse genetics, and the resulting mutant virus was viable and replicated as efficiently as wild-type virus in cells with a defective IFN response. However, mutant virus replication was strongly attenuated in cells with an intact IFN response. Thus, nsp1 is likely a virulence factor that contributes to pathogenicity by favoring SARS-CoV replication

Reverse Genetic Analysis of the Transcription Regulatory Sequence of the Coronavirus Transmissible Gastroenteritis Virus

Coronavirus discontinuous transcription uses a highly conserved sequence (CS) in the joining of leader and body RNAs. Using a full-length infectious construct of transmissable gastroenteritis virus, the present study demonstrates that subgenomic transcription is heavily influenced by upstream flanking sequences and supports a mechanism of transcription attenuation that is regulated in part by a larger domain composed of primarily upstream flanking sequences which select appropriately positioned CS elements for synthesis of subgenomic RNAs