Publisher Correction: Npj Viruses, volume 2, missing Data Availability statements
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Influenza B viruses are more susceptible to high temperatures than influenza A viruses
Seasonal influenza is caused by two subtypes of influenza A virus (A/H1N1 and A/H3N2) and two lineages of influenza B viruses (B/Victoria-lineage and B/Yamagata-lineage). Seasonal influenza viruses replicate efficiently in the human upper respiratory tract, where the temperature is 33 °C. In this study, we investigated the susceptibility of seasonal influenza A and B viruses to different temperatures. We examined the differences in viral replication efficiency inside cultured cells and in infectious titre outside cultured cells at different temperatures (i.e., 33 °C, 37 °C, and 39 °C). We found that there were differences in temperature sensitivity between influenza A and B viruses, with influenza B viruses being more temperature sensitive. In addition, we found that cells cultured at 39 °C and infected with influenza B virus showed decreased expression of HA protein with receptor-binding activity on the cell surface. Our findings contribute to our understanding of the properties of seasonal influenza viruses.
Molecular imaging of viral pathogenesis and opportunities for the future
Molecular imaging is used in clinical and research settings. Since tools to study viral pathogenesis longitudinally and systemically are limited, molecular imaging is an attractive and largely unexplored tool. This review discusses molecular imaging probes and techniques for studying viruses, particularly those currently used in oncology that are applicable to virology. Expanding the repertoire of probes to better detect viral disease may make imaging even more valuable in (pre-)clinical settings.
Pathogenesis and transmission of SARS-CoV-2 D614G, Alpha, Gamma, Delta, and Omicron variants in golden hamsters
Since the emergence of SARS-CoV-2 in humans, novel variants have evolved to become dominant circulating lineages. These include D614G (B.1 lineage), Alpha (B.1.1.7), Gamma (P.1), Delta (B.1.617.2), and Omicron BA.1 (B.1.1.529) and BA.2 (B.1.1.529.2) viruses. Here, we compared the viral replication, pathogenesis, and transmissibility of these variants. Replication kinetics and innate immune response against the viruses were tested in ex vivo human nasal epithelial cells (HNEC) and induced pluripotent stem cell-derived lung organoids (IPSC-LOs), and the golden hamster model was employed to test pathogenicity and potential for transmission by the respiratory route. Delta, BA.1, and BA.2 viruses replicated more efficiently, and outcompeted D614G, Alpha, and Gamma viruses in an HNEC competition assay. BA.1 and BA.2 viruses, however, replicated poorly in IPSC-LOs compared to other variants. Moreover, BA.2 virus infection significantly increased secretion of IFN-λ1, IFN-λ2, IFN-λ3, IL-6, and IL-1RA in HNECs relative to D614G infection, but not in IPSC-LOs. The BA.1 and BA.2 viruses replicated less effectively in hamster lungs compared to the other variants; and while the Gamma virus reached titers comparable to D614G and Delta viruses, it caused greater lung pathology. Lastly, the Gamma and Delta variants transmitted more efficiently by the respiratory route compared to the other viruses, while BA.1 and BA.2 viruses transmitted less efficiently. These findings demonstrate the ongoing utility of experimental risk assessment as SARS-CoV-2 variants continue to evolve.
Genomic and transcriptomic insights into complex virus–prokaryote interactions in marine biofilms
Marine biofilms are complex communities of microorganisms that play a crucial ecological role in oceans. Although prokaryotes are the dominant members of these biofilms, little is known about their interactions with viruses. By analysing publicly available and newly sequenced metagenomic data, we identified 2446 virus–prokaryote connections in 84 marine biofilms. Most of these connections were between the bacteriophages in the Uroviricota phylum and the bacteria of Proteobacteria, Cyanobacteria and Bacteroidota. The network of virus–host pairs is complex; a single virus can infect multiple prokaryotic populations or a single prokaryote is susceptible to several viral populations. Analysis of genomes of paired prokaryotes and viruses revealed the presence of 425 putative auxiliary metabolic genes (AMGs), 239 viral genes related to restriction–modification (RM) systems and 38,538 prokaryotic anti-viral defence-related genes involved in 15 defence systems. Transcriptomic evidence from newly established biofilms revealed the expression of viral genes, including AMGs and RM, and prokaryotic defence systems, indicating the active interplay between viruses and prokaryotes. A comparison between biofilms and seawater showed that biofilm prokaryotes have more abundant defence genes than seawater prokaryotes, and the defence gene composition differs between biofilms and the surrounding seawater. Overall, our study unveiled active viruses in natural biofilms and their complex interplay with prokaryotes, which may result in the blooming of defence strategists in biofilms. The detachment of bloomed defence strategists may reduce the infectivity of viruses in seawater and result in the emergence of a novel role of marine biofilms.
20 years of research on giant viruses
Some twenty years ago, the discovery of the first giant virus, Acanthamoeba polyphaga mimivirus (now mimivirus bradfordmassiliense species), paved the way for the discovery of more than 10 new families of protist-infecting DNA viruses with unexpected diversity in virion shape and size, gene content, genome topology and mode of replication. Following their brief description, we examine how the historical concepts of virology have held up in the light of this new knowledge. Although the initial emphasis was on the gigantism of the newly described viruses infecting amoebae, the subsequent discovery of viruses with intermediate virion and genome sizes gradually re-established a continuum between the smallest and largest viruses within the phylum Nucleocytoviricota.
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