Background The full range of long-term health consequences of COVID-19 in patients who are discharged from hospital is largely unclear. The aim of our study was to comprehensively compare consequences between 6 months and 12 months after symptom onset among hospital survivors with COVID-19. MethodsWe undertook an ambidirectional cohort study of COVID-19 survivors who had been discharged from Jin Yin-tan Hospital (Wuhan, China) between Jan 7 and May 29, 2020. At 6-month and 12-month follow-up visit, survivors were interviewed with questionnaires on symptoms and health-related quality of life (HRQoL), and received a physical examination, a 6-min walking test, and laboratory tests. They were required to report their health-care use after discharge and work status at the 12-month visit. Survivors who had completed pulmonary function tests or had lung radiographic abnormality at 6 months were given the corresponding tests at 12 months. Non-COVID-19 participants (controls) matched for age, sex, and comorbidities were interviewed and completed questionnaires to assess prevalent symptoms and HRQoL. The primary outcomes were symptoms, modified British Medical Research Council (mMRC) score, HRQoL, and distance walked in 6 min (6MWD). Multivariable adjusted logistic regression models were used to evaluate the risk factors of 12-month outcomes. Findings 1276 COVID-19 survivors completed both visits. The median age of patients was 59•0 years (IQR 49•0-67•0) and 681 (53%) were men. The median follow-up time was 185•0 days (IQR 175•0-198•0) for the 6-month visit and 349•0 days (337•0-361•0) for the 12-month visit after symptom onset. The proportion of patients with at least one sequelae symptom decreased from 68% (831/1227) at 6 months to 49% (620/1272) at 12 months (p<0•0001). The proportion of patients with dyspnoea, characterised by mMRC score of 1 or more, slightly increased from 26% (313/1185) at 6-month visit to 30% (380/1271) at 12-month visit (p=0•014). Additionally, more patients had anxiety or depression at 12-month visit (26% [331/1271] at 12-month visit vs 23% [274/1187] at 6-month visit; p=0•015). No significant difference on 6MWD was observed between 6 months and 12 months. 88% (422/479) of patients who were employed before COVID-19 had returned to their original work at 12 months. Compared with men, women had an odds ratio of 1•43 (95% CI 1•04-1•96) for fatigue or muscle weakness, 2•00 (1•48-2•69) for anxiety or depression, and 2•97 (1•50-5•88) for diffusion impairment. Matched COVID-19 survivors at 12 months had more problems with mobility, pain or discomfort, and anxiety or depression, and had more prevalent symptoms than did controls.Interpretation Most COVID-19 survivors had a good physical and functional recovery during 1-year follow-up, and had returned to their original work and life. The health status in our cohort of COVID-19 survivors at 12 months was still lower than that in the control population.

Despite the worldwide distribution, most of the known Seoul viruses (SEOV) are closely related to each other. In this study, the M and the S segment sequences of SEOV were recovered from 130 lung tissue samples (mostly of Norway rats) and from six patient serum samples by reverse transcription-PCR. Genetic analysis revealed that all sequences belong to SEOV and represent 136 novel strains. Phylogenetic analysis of all available M and S segment sequences of SEOV, including 136 novel Chinese strains, revealed four distinct groups. All non-Chinese SEOV strains and most of the Chinese variants fell into the phylogroup A, while the Chinese strains originating from mountainous areas clustered into three other distinct groups (B, C, and D). We estimated that phylogroup A viruses may have arisen only within the last several centuries. All non-Chinese variants appeared to be directly originated from China. Thus, phylogroup A viruses distributed worldwide may share a recent ancestor, whereas SEOV seems to be as diversified genetically as other hantaviruses. In addition, all available mitochondrial DNA (mtDNA) sequences of Norway rats, including our 44 newly recovered mtDNA sequences, were divided into two phylogenetic groups. The first group, which is associated with the group A SEOV variants, included most of rats from China and also all non-Chinese rats, while the second group consisted of a few rats originating only from mountain areas in China. We hypothesize that an ancestor of phylogroup A SEOV variants was first exported from China to Europe and then spread through the New World following the migration of Norway rats.

Respiratory syncytial virus (RSV) is an important etiological agent of respiratory infection in children for which no specific treatment option is available. The RSV virion contains two surface glycoproteins (F and G) that are vital for the initial phases of infection, making them critical targets for RSV therapeutics. Recent studies have identified the broad-spectrum antiviral properties of silver nanoparticles (AgNPs) against respiratory pathogens, such as adenovirus, parainfluenza, and influenza. AgNPs achieve this by attaching to viral glycoproteins, blocking entry into the host cell. The objective of this study was to evaluate the antiviral and immunomodulatory effects of AgNPs in RSV infection. Herein we demonstrate AgNP-mediated reduction in RSV replication, both in epithelial cell lines and in experimentally infected BALB/c mice. Marked reduction in pro-inflammatory cytokines (i.e., IL-1α, IL-6, TNF-α) and pro-inflammatory chemokines (i.e., CCL2, CCL3, CCL5) was also observed. Conversely, CXCL1, G-CSF, and GM-CSF were increased in RSV-infected mice treated with AgNPs, consistent with an increase of neutrophil recruitment and activation in the lung tissue. Following experimental antibody-dependent depletion of neutrophils, the antiviral effect of AgNPs in mice treated was ablated. To our knowledge, this is the first in vivo report demonstrating antiviral activity of AgNPs during RSV infection.

We have identified host IQGAP1 as an interacting partner for Ebola virus (EBOV) VP40, and its expression is required for EBOV VP40 virus-like particle (VLP) budding. IQGAP1 is involved in actin cytoskeletal remodeling during cell migration and formation of filopodia. The physical interaction and the functional requirement for IQGAP1 in EBOV VP40 VLP egress link virus budding to the cytoskeletal remodeling machinery. Consequently, this interaction represents a novel target for development of therapeutics to block budding and transmission of filoviruses. E bola virus (EBOV) and Marburg virus (MARV) are enveloped, negative-sense RNA viruses belonging to the family Filoviridae which cause hemorrhagic syndromes with high mortality rates in humans (1, 2). There are currently no licensed vaccines or therapeutics to control filovirus infection and transmission. The filovirus VP40 matrix protein plays a central role in virion assembly and egress such that independent expression of VP40 leads to the production of virus-like particles (VLPs) that accurately mimic budding of live virus (3-7). Late (L) budding domains of VP40, which recruit host proteins (e.g., Tsg101) required for efficient virus-cell separation (or "pinching-off"), consist of core consensus amino acid motifs such as PPxY, P(T/S)AP, YxxL, or FPIV (x ϭ any amino acid). The conservation of L-domains within matrix proteins of many RNA viruses suggests that they are generally important and required for efficient RNA virus budding (8), although they are not absolutely required for viral replication (9).Unlike the events that contribute to the late stages of filovirus budding, little is known about the regulation of early stages of filovirus budding, but this likely involves cellular mechanisms that control cytoskeletal remodeling and membrane deformation/curvature. For example, filopodia significantly increase the ability of filoviruses to spread from cell to cell, thereby contributing to pathogenesis (10). One multifunctional host protein that plays key roles in regulating cell motility, cytoskeletal architecture, actin polymerization, and formation of filopodia is IQGAP1 (11-16). Indeed, IQGAP1 is a widely expressed scaffolding protein with multiple proteinprotein interaction domains, including a WW-domain that may interact with viral PPxY type L-domains (12). Intriguingly, IQGAP1 has been detected in purified HIV-1 virions (17) and has been shown to interact with the Gag protein of Moloney murine leukemia virus (MuLV) (18) and the core protein of classical swine fever virus (CSFV) (19) as well as host Tsg101 (20).Here we investigated whether endogenous IQGAP1 interacts with EBOV VP40 and whether this interaction regulates efficient egress of EBOV VP40 VLPs. We found that EBOV VP40 interacts with endogenous IQGAP1 and that the L-domain region of VP40 mediates this interaction. Importantly, we found that egress of EBOV VP40 VLPs from IQGAP1-suppressed cells is reduced. Together, our findings identify a functional requirement for IQGAP1 interactions with EBOV VP...

16/19) of the ALV-J layer isolates displayed less than 92.5% sequence homology to those of the ALV-J broiler isolates, although the transcriptional regulatory elements that are typical of avian retroviruses were highly conserved. Several unique nucleotide substitutions in the env gene, the U3 region, and the E element of most of the ALV-J layer isolates were detected. These results suggested that the env gene, E element, and U3 region in the ALV-J layer isolates have evolved rapidly and were significantly different from those of the ALV-J broiler isolates. These findings will contribute to a better understanding of the pathogenic mechanism of layer tumor diseases induced by ALV-J.

Some studies found that there was a significant association between asthma and the risk of lung cancer. However, the results are inconclusive. Therefore, we performed a meta-analysis. We searched the electronic databases for all relevant articles. Odds ratio (OR) with 95% confidence interval (CI) were used to calculate the strength of the association between asthma and lung cancer risk. Asthma was significantly associated with the increased risk of lung cancer (OR = 1.44; 95% CI 1.31–1.59; P < 0.00001; I2 = 83%). Additionally, asthma patients without smoking also had the increased lung cancer risk. In the subgroup analysis of race and gender, Caucasians, Asians, male, and female patients with asthma showed the increased risk of lung cancer. However, asthma was not significantly associated with lung adenocarcinoma risk. In the stratified analysis by asthma definition, significant associations were found between asthma and lung cancer in self-reported subgroup, questionnaire subgroup, and register databases subgroup. However, no significant association was observed in physician-diagnosed asthma subgroup. In conclusion, this meta-analysis suggested that asthma might be significantly associated with lung cancer risk.

The emergence and spread of Type 2 Porcine Reproductive and Respiratory Syndrome virus (Type 2 PRRSV) in North America is heavily influenced by the multiple site production system used in the hog industry. However, it is unclear how anthropogenic factors such has this have shaped the current spatial distribution of PRRSV genotypes. We employed Bayesian phylogeographic analyses of 7040 ORF5 sequences to reveal the recent geographical spread of Type 2 PRRSV in North America. The directions and intensities in our inferred virus traffic network closely mirror the hog transportation. Most notably, we reveal multiple viral introductions from Canada into the United States causing a major shift in virus genetic composition in the Midwest USA that went unnoticed by the regular surveillance and field epidemiological studies. Overall, these findings provide important insights into the dynamics of Type 2 PRRSV evolution and spread that will facilitate programs for control and prevention.

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