Effect Of Virus Infection Research Articles

Fatal attraction: Dengue Virus and the Mitochondrial Connection

Viruses rely on host cell machinery, an obligation that forces a myriad of interactions between the viral proteins and host cell organelles to create an intracellular environment conducive to viral dissemination. In their pursuit to exploit the cellular organelles and modulate their function, viruses affect the overall physiology of the cell. The consequence of viral infection on host cell physiology largely varies between acute vs chronic infection, cell type infected, and the productive or abortive nature of the infection. Viruses leading to chronic infection favor viral persistence by promoting the viability of infected cells by inducing cellular homeostatic pathways. In contrast, viruses causing an acute infection trigger physiological alterations that often lead to the cytocidal effect.

Antiviral effects of Atractyloside A on the influenza B virus (Victoria strain) infection.

Influenza viruses pose a serious threat to human health, infecting hundreds of millions of people worldwide each year, resulting in a significant increase in global morbidity and mortality. Influenza activity has declined at the onset of the COVID-19 pandemic, but the genetic diversity of B/Victoria lineage viruses has increased significantly during this period. Therefore, the prevention and treatment of the influenza B Victoria strain virus should continue to attract research attention. In this study, we found that Atractyloside A (AA), one of the effective components in Atractylodes lancea (Thunb.) DC shows potential antiviral properties. This study shows that AA not only possesses anti-influenza B virus infection effects in vivo and in vitro but also can regulate macrophage polarization to the M2 type, which can effectively attenuate the damage caused by influenza B virus infection. Therefore, Atractyloside A may be an effective natural drug against B/Victoria influenza infection.

HIV Infection, Chromosome Instability, and Micronucleus Formation.

Genome integrity is critical for proper cell functioning, and chromosome instability can lead to age-related diseases, including cancer and neurodegenerative disorders. Chromosome instability is caused by multiple factors, including replication stress, chromosome missegregation, exposure to pollutants, and viral infections. Although many studies have investigated the effects of environmental or lifestyle genotoxins on chromosomal integrity, information on the effects of viral infections on micronucleus formation and other chromosomal aberrations is still limited. Currently, HIV infection is considered a chronic disease treatable by antiretroviral therapy (ART). However, HIV-infected individuals still face important health problems, such as chronic inflammation and age-related diseases. In this context, this article reviews studies that have evaluated genomic instability using micronucleus assays in the context of HIV infection. In brief, HIV can induce chromosome instability directly through the interaction of HIV proteins with host DNA and indirectly through chronic inflammation or as a result of ART use. Connections between HIV infection, immunosenescence and age-related disease are discussed in this article. The monitoring of HIV-infected individuals should consider the increased risk of chromosome instability, and lifestyle interventions, such as reduced exposure to genotoxins and an antioxidant-rich diet, should be considered. Therapies to reduce chronic inflammation in HIV infection are needed.

Pan-viral serology defines hepatocellular carcinoma's response to immunotherapy

Background: Hepatocellular carcinoma (HCC) is the leading cause of liver cancer and survival remains low due to poor treatment response. Surgery is the current first-line therapy for eligible candidates; however, patients relapse despite curative resection or require systemic treatment for advanced disease. Immune checkpoint inhibition (ICI) therapy has recently shown promise in the treatment of cancers, including HCC; yet, we do not know which patients may benefit. Additionally, the effect of viral infection on host long-term health and how the immune footprint left by viruses may impact immunotherapy response have not been explored. We hypothesized that viral infection alters host immunity in subtle ways, leaving a persistent footprint on the immune system, which may contribute to patient response to ICI.

Коронавирусная инфекция и дислипидемия — есть ли связь?

Dyslipidemia is one of the most common comorbidities in patients infected with the SARS-CoV-2 coronavirus. In this review based on the up- to-date publications the authors assess the potential impact of dyslipidemia on the clinical course and prognosis in COVID-19 infected patients, as well as the viral infection effects on the lipid profile in patients with dyslipidemia. The COVID-19 driven inflammatory response leads to an increase in high-density lipoprotein (HDL) levels, modulation of apolipoproteins, increase in serum amyloid protein A concentration, and a decrease in apolipoprotein A-I, M and E levels, thus affecting the antioxidant, anti-inflammatory and immunomodulatory properties of HDL. The use of statins in patients with COVID-19 may mitigate the risk of lipid disorders. By inhibiting endogenous cholesterol synthesis, statins reduce its amount in lipid rafts and therefore may limit the entry of the SARS-CoV-2 virus into host cells. Moreover, statins, by reducing the overexpression of proinflammatory cytokines, can counteract COVID-19-associated cytokine storm. KEYWORDS: COVID-19, dyslipidemia, obesity, treatment, lipoproteins, statins, fibrates. FOR CITATION: Akhmedov V.A. Coronavirus disease and dyslipidemia — is there an association? Russian Medical Inquiry. 2023;7(1):36– 40 (in Russ.). DOI: 10.32364/2587-6821-2023-7-1-36-40.

Sentiment Analysis of Insomnia-Related Tweets via a Combination of Transformers Using Dempster-Shafer Theory: Pre- and Peri-COVID-19 Pandemic Retrospective Study.

The COVID-19 pandemic has imposed additional stress on population health that may result in a change of sleeping behavior. In this study, we hypothesized that using natural language processing to explore social media would help with assessing the mental health conditions of people experiencing insomnia after the outbreak of COVID-19. We designed a retrospective study that used public social media content from Twitter. We categorized insomnia-related tweets based on time, using the following two intervals: the prepandemic (January 1, 2019, to January 1, 2020) and peripandemic (January 1, 2020, to January 1, 2021) intervals. We performed a sentiment analysis by using pretrained transformers in conjunction with Dempster-Shafer theory (DST) to classify the polarity of emotions as positive, negative, and neutral. We validated the proposed pipeline on 300 annotated tweets. Additionally, we performed a temporal analysis to examine the effect of time on Twitter users' insomnia experiences, using logistic regression. We extracted 305,321 tweets containing the word insomnia (prepandemic tweets: n=139,561; peripandemic tweets: n=165,760). The best combination of pretrained transformers (combined via DST) yielded 84% accuracy. By using this pipeline, we found that the odds of posting negative tweets (odds ratio [OR] 1.39, 95% CI 1.37-1.41; P<.001) were higher in the peripandemic interval compared to those in the prepandemic interval. The likelihood of posting negative tweets after midnight was 21% higher than that before midnight (OR 1.21, 95% CI 1.19-1.23; P<.001). In the prepandemic interval, while the odds of posting negative tweets were 2% higher after midnight compared to those before midnight (OR 1.02, 95% CI 1.00-1.07; P=.008), they were 43% higher (OR 1.43, 95% CI 1.40-1.46; P<.001) in the peripandemic interval. The proposed novel sentiment analysis pipeline, which combines pretrained transformers via DST, is capable of classifying the emotions and sentiments of insomnia-related tweets. Twitter users shared more negative tweets about insomnia in the peripandemic interval than in the prepandemic interval. Future studies using a natural language processing framework could assess tweets about other types of psychological distress, habit changes, weight gain resulting from inactivity, and the effect of viral infection on sleep.

RNA virus infections and their effect on host alternative splicing

It is evident that viral infection dramatically alters host gene expression, and these alterations have both pro- and anti-viral functions. While the effects of viral infection on transcription and translation have been comprehensively reviewed, less attention has been paid to the impact on alternative splicing of pre-messenger RNAs. Here we review salient examples of how viral infection leads to changes in alternative splicing and discuss how these changes impact infection.

Differential effects of Usutu and West Nile viruses on neuroinflammation, immune cell recruitment and blood–brain barrier integrity

ABSTRACT Usutu (USUV) and West Nile (WNV) viruses are two closely related Flavivirus belonging to Japanese encephalitis virus serogroup. Evidence of increased circulation of these two arboviruses now exist in Europe. Neurological disorders are reported in humans mainly for WNV, despite the fact that the interaction and effects of viral infections on the neurovasculature are poorly described, notably for USUV. Using a human in vitro blood–brain barrier (BBB) and a mouse model, this study characterizes and compares the cerebral endothelial cell permissiveness, innate immunity and inflammatory responses and immune cell recruitment during infection by USUV and WNV. Both viruses are able to infect and cross the human BBB but with different consequences. We observed that WNV infects BBB cells resulting in significant endothelium impairment, potent neuroinflammation and immune cell recruitment, in agreement with previous studies. USUV, despite being able to infect BBB cells with higher replication rate than WNV, does not strongly affect endothelium integrity. Importantly, USUV also induces neuroinflammation, immune cell recruitment such as T lymphocytes, monocytes and dendritic cells (DCs) and was able to infect dendritic cells (DCs) more efficiently compared to WNV, with greater propensity for BBB recruitment. DCs may have differential roles for neuroinvasion of the two related viruses.

Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis.

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). Compared to other types of self-limiting myelin disorders, MS compartmentalizes and maintains chronic inflammation in the CNS. Even though the exact cause of MS is unclear, it is assumed that genetic and environmental factors play an important role in susceptibility to this disease. The progression of MS is triggered by certain environmental factors, such as viral infections. The most important viruses that affect MS are Epstein-Barr virus (EBV), human herpes virus 6 (HHV-6), human endogenous retrovirus (HERV), cytomegalovirus (CMV), and varicella zoster virus (VZV). These viruses all have latent stages that allow them to escape immune detection and reactivate after exposure to various stimuli. Furthermore, their tropism for CNS and immune system cells explains their possible deleterious function in neuroinflammation. In this study, the effect of viral infections on MS disease focuses on the details of viruses that can change the risk of the disease. Paying attention to the most recent articles on the role of SARS-CoV-2 in MS disease, laboratory indicators show the interaction of the immune system with the virus. Also, strategies to prevent viruses that play a role in triggering MS are discussed, such as EBV, which is one of the most important.

Alterations of the Mucosal Immune Response and Microbial Community of the Skin upon Viral Infection in Rainbow Trout (Oncorhynchus mykiss).

The skin is the largest organ on the surface of vertebrates, which not only acts as the first line of defense against pathogens but also harbors diverse symbiotic microorganisms. The complex interaction between skin immunity, pathogens, and commensal bacteria has been extensively studied in mammals. However, little is known regarding the effects of viral infection on the skin immune response and microbial composition in teleost fish. In this study, we exposed rainbow trout (Oncorhynchus mykiss) to infectious hematopoietic necrosis virus (IHNV) by immersion infection. Through pathogen load detection and pathological evaluation, we confirmed that IHNV successfully invaded the rainbow trout, causing severe damage to the epidermis of the skin. qPCR analyses revealed that IHNV invasion significantly upregulated antiviral genes and elicited strong innate immune responses. Transcriptome analyses indicated that IHNV challenge induced strong antiviral responses mediated by pattern recognition receptor (PRR) signaling pathways in the early stage of the infection (4 days post-infection (dpi)), and an extremely strong antibacterial immune response occurred at 14 dpi. Our 16S rRNA sequencing results indicated that the skin microbial community of IHNV-infected fish was significantly richer and more diverse. Particularly, the infected fish exhibited a decrease in Proteobacteria accompanied by an increase in Actinobacteria. Furthermore, IHNV invasion favored the colonization of opportunistic pathogens such as Rhodococcus and Vibrio on the skin, especially in the later stage of infection, leading to dysbiosis. Our findings suggest that IHNV invasion is associated with skin microbiota dysbiosis and could thus lead to secondary bacterial infection.

High temporal resolution Nanopore sequencing dataset of SARS-CoV-2 and host cell RNAs.

BackgroundRecent studies have disclosed the genome, transcriptome, and epigenetic compositions of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the effect of viral infection on gene expression of the host cells. It has been demonstrated that, besides the major canonical transcripts, the viral genome also codes for noncanonical RNA molecules. While the structural characterizations have revealed a detailed transcriptomic architecture of the virus, the kinetic studies provided poor and often misleading results on the dynamics of both the viral and host transcripts due to the low temporal resolution of the infection event and the low virus/cell ratio (multiplicity of infection [MOI] = 0.1) applied for the infection. It has never been tested whether the alteration in the host gene expressions is caused by aging of the cells or by the viral infection.FindingsIn this study, we used Oxford Nanopore's direct cDNA and direct RNA sequencing methods for the generation of a high-coverage, high temporal resolution transcriptomic dataset of SARS-CoV-2 and of the primate host cells, using a high infection titer (MOI = 5). Sixteen sampling time points ranging from 1 to 96 hours with a varying time resolution and 3 biological replicates were used in the experiment. In addition, for each infected sample, corresponding noninfected samples were employed. The raw reads were mapped to the viral and to the host reference genomes, resulting in 49,661,499 mapped reads (54,62 Gbs). The genome of the viral isolate was also sequenced and phylogenetically classified.ConclusionsThis dataset can serve as a valuable resource for profiling the SARS-CoV-2 transcriptome dynamics, the virus–host interactions, and the RNA base modifications. Comparison of expression profiles of the host gene in the virally infected and in noninfected cells at different time points allows making a distinction between the effect of the aging of cells in culture and the viral infection. These data can provide useful information for potential novel gene annotations and can also be used for studying the currently available bioinformatics pipelines.

Measles virus-imposed remodeling of the autophagy machinery determines the outcome of bacterial coinfection

ABSTRACT Although it is admitted that secondary infection can complicate viral diseases, the consequences of viral infection on cell susceptibility to other infections remain underexplored at the cellular level. We though to examine whether the sustained macroautophagy/autophagy associated with measles virus (MeV) infection could help cells oppose invasion by Salmonella Typhimurium, a bacterium sensitive to autophagic restriction. We report here the unexpected finding that Salmonella markedly replicated in MeV-infected cultures due to selective growth within multinucleated cells. Hyper-replicating Salmonella localized outside of LAMP1-positive compartments to an extent that equaled that of the predominantly cytosolic sifA mutant Salmonella. Bacteria were subjected to effective ubiquitination but failed to be targeted by LC3 despite an ongoing productive autophagy. Such a phenotype could not be further aggravated upon silencing of the selective autophagy regulator TBK1 or core autophagy factors ATG5 or ATG7. MeV infection also conditioned primary human epithelial cells for augmented Salmonella replication. The analysis of selective autophagy receptors able to target Salmonella revealed that a lowered expression level of SQSTM1/p62 and TAX1BP1/T6BP autophagy receptors prevented effective anti-Salmonella autophagy in MeV-induced syncytia. Conversely, as SQSTM1/p62 is promoting the cytosolic growth of Shigella flexneri, MeV infection led to reduced Shigella replication. The results indicate that the rarefaction of dedicated autophagy receptors associated with MeV infection differentially affects the outcome of bacterial coinfection depending on the nature of the functional relationship between bacteria and such receptors. Thus, virus-imposed reconfiguration of the autophagy machinery can be instrumental in determining the fate of bacterial coinfection.Abbreviations:ACTB/β-ACTIN: actin beta; ATG: autophagy related; BAFA1: bafilomycin A1; CFU: colony-forming units; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; FIP: fusion inhibitory peptide; GFP: green fluorescent protein; LAMP1: lysosomal associated membrane protein 1; LIR: MAP1LC3/LC3-interacting region; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MeV: measles virus; MOI: multiplicity of infection; OPTN: optineurin; PHH: primary human hepatocyte; SCV: Salmonella-containing vacuoles; SQSTM1/p62: sequestosome 1; S. flexneri: Shigella flexneri; S. Typhimurium: Salmonella enterica serovar Typhimurium; TAX1BP1/T6BP: Tax1 binding protein 1; TBK1: TANK binding kinase 1

Role of MicroRNAs in the Development of Chronic Liver Disease in Hepatitis Virus-Infected Egyptian Population

Background: The identification of miRNAs that play a role in the regulation of the viral life cycle and its related liver illness opens the door to the development of diagnostic biomarkers that can categorize patients at higher risk for developing end-stage liver disease. This study was designed to investigate the role of miRNAs in the development of viral hepatitis-induced chronic liver disease (CLD) in the Egyptian population, as well as their potential as possible diagnostic biomarkers for chronic hepatitis virus infection.&#x0D; Methodology: The study involved 100 CLD patients; 55 cases of hepatitis C virus (HCV) and 45 cases of non-viral hepatitis, in addition to 40 healthy controls. The expression of five miRNAs (miR‐30, miR‐122, miR‐296, miR‐351, and miR‐431) was assessed using real-time PCR.&#x0D; Results: Serum levels of miR‐30, miR‐122, miR‐296, miR‐351, and miR‐431 were significantly higher in all patients than the control group (p&lt;0.01). Also, they were significantly greater in viral hepatitis cases compared to the non-viral hepatitis group (p&lt;0.01). The sensitivities and specificities of miR-122a, miR‐30, miR‐296, miR‐351, and miR‐431 were (85.71%, 83.33%), (82.35%, 83.33%), (85.71%, 69.44%), (88.64%, 75.76%), and (87.80%, 65.79%), respectively.&#x0D; Conclusions: miR‐30, miR‐122, miR‐296, miR‐351, and miR‐431 play key roles in the development of CLD as a consequence of viral infection. So, they have the potential to be targeted for the early detection of chronic hepatitis virus infection and allow for exploring a new frontier in the discovery of innovative therapeutics to combat chronic viral infection and its serious life-threatening complications including liver cancer.

EFFECT OF YELLOW VEIN MOSAIC VIRUS DISEASE OF OKRA ON GROWTH AND PROXIMATE ANALYSIS OF SOME OKRA CULTIVARS IN DUTSIN-MA

The study was conducted on okra, an important food consumed in Dutsin ma, Katsina State, Nigeria. Reports have indicates the effect of viral infections on produce quantity and quality, this study determined and document the effect of yellow vein mosaic virus disease of okra on performance and nutritional composition of some okra cultivars in Dutsin-ma, Sudan Savannah. Seedlings were inoculated with the virus at 1 week post emergence. Each cultivar was evaluated as inoculated (infected) and uninoculated (Healthy) treatments. Percent disease severity of infection (%), yield related parameters and proximate analysis of pod were measured. Data were subjected to independent t test and significance was determined at 5 % level of probability. Percent disease severity was highest in ‘Yar Balla’ (21.3%) as compared to the remaining cultivars. Reductions in plant height (8.8 %), fruit weight (37.6 %) and crude protein were significantly lower in ‘Yar Balla’ and ‘Jikin Mutum’ The present study reveal that the reduction in crude protein as a result of YVMV infection would worsen the protein deficiency problem of the populace who depend on the crop as the cheapest means of obtaining their daily protein and mineral requirement. There is therefore the need to prevent viral infection of vegetable crops in order to ensure high yield and guarantee its nutritive value.

Metagenomic next-generation sequencing for identifying pathogens in patients with rheumatic diseases and diffuse pulmonary lesions: A retrospective diagnostic study.

ObjectiveLung involvement is a major cause of morbidity and mortality in patients with rheumatic diseases. This study aimed to assess the application value of metagenomic next-generation sequencing (mNGS) for identifying pathogens in patients with rheumatic diseases and diffuse pulmonary lesions.MethodsThis retrospective study included patients who were diagnosed with rheumatic diseases and presenting diffuse pulmonary lesions on chest radiography in Xiangya Hospital from July 2018 to May 2022. Clinical characteristics were summarized, including demographics, symptoms, comorbidities, radiological and laboratory findings, and clinical outcomes. Pulmonary infection features of these patients were analyzed. Furthermore, diagnostic performance of mNGS and conventional methods (including smear microscopy, culture, polymerase chain reaction assay, and serum immunological test) in identifying pulmonary infections and causative pathogens were compared.ResultsA total of 98 patients were included, with a median age of 58.0 years old and a female proportion of 59.2%. Of these patients, 71.4% showed the evidence of pulmonary infections. Combining the results of mNGS and conventional methods, 129 infection events were detected, including 45 bacterial, 40 fungal and 44 viral infection events. Pulmonary mixed infections were observed in 38.8% of patients. The detection rates of mNGS for any pathogen (71.4% vs 40.8%, P < 0.001) and mixed pathogens (40.8% vs 12.2%, P < 0.001) were higher than that of conventional methods. Moreover, mNGS had a significantly higher sensitivity (97.1% vs. 57.1%, P < 0.001) than conventional methods in identifying pulmonary infections, while its specificity (92.9% vs. 96.4%, P = 0.553) were comparable to conventional methods. Antimicrobial and antirheumatic treatments were markedly modified based on mNGS results in patients with rheumatic diseases and diffuse pulmonary lesions.ConclusionsFor patients diagnosed with rheumatic diseases and presenting diffuse pulmonary lesions, mNGS is a powerful complement to conventional methods in pathogen identification due to its high efficiency and broad spectrum. Early application of mNGS can provide guidance for precision treatment, and may reduce mortality and avoid antibiotic abuse.

BIOCHEMICAL CHANGES IN LEAVES OF RESISTANT AND SUSCEPTIBLE URDBEAN GENOTYPES INFECTED WITH URDBEAN LEAF CRINKLE VIRUS (ULCV)

Urdbean leaf crinkle virus (ULCV) is a widespread and most destructive virus that causes leaf crinkle disease in black gram. Virus infection causes alteration in physiological and biochemical processes within the plant. In present study, effect of viral infection was investigated on chlorophyll content, total soluble sugar, total protein, phenolic contents, sodium dismutase (SOD) and nitrate reductase activities in the leaves of susceptible and resistant genotypes of urdbean at 30 days after virus inoculation. Disease symptoms were mild (6.7% to 10%) in resistant genotypes and severe (36% to 43%) in susceptible genotypes. ULCV infection resulted in a significant decrease in chlorophyll content in infected plants of all genotypes over control plants; however, magnitude of reduction was more in susceptible genotypes (41%) as compared to the resistant genotypes (14.35%). The total sugar and protein contents were significantly higher in the inoculated susceptible (210.26 % and 68.67%, respectively) as compared to the resistant genotypes (183.87% and 25.89%, respectively). Also, the total phenolic content was significantly higher in inoculated resistant genotypes (83.91%) over the susceptible genotypes (25.89%). There was significant decrease in the activity of superoxide dismutase enzyme in resistant genotypes as compared to susceptible inoculated genotypes. Similarly, a reduction in nitrate reductase activity was more in inoculated plants of resistant genotypes. Our results indicate that post-infection significant increases in total sugars and proteins in susceptible genotypes and phenols in resistant genotypes may have a role in disease resistance and development. Changes in enzymatic activities in resistant and susceptible genotypes might also have some role in resistance against ULCV.

O-140 The impact of past COVID-19 infection on pregnancy rates in frozen embryo transfer cycles

Study questionWhat is the effect of COVID-19 infection on pregnancy rates in frozen embryo transfer (FET) cycles?Summary answerPast COVID-19 infection decreased pregnancy rates in FET cycles, especially in patients with recent infection.What is known alreadyACE2 and TMPRSS2 are expressed in the endometrium, potentially enabling SARS-COV-2 viral invasion of the cells. Unlike with bacterial infections, the effect of viral infections in general on implantation and pregnancy rates is unclear. Some evidence suggests that early embryonic and trophoblastic infection, may result in impaired implantation or placentation. A recently published study including both recovered and vaccinated patients did not find an effect of COVID-19 immunity on FET cycle outcomes. The study did not stratify by time from infection thus the immediate consequences of infection on pregnancy rates could not be properly evaluated.Study design, size, durationA retrospective cohort study, including 41 COVID-19 recovered women, aged 20-42 years that underwent FET cycles, and 41 controls between January 1, and June 31, 2021, at a large IVF unit.Participants/materials, setting, methodsEmbryos transferred were the product of fresh cycles performed prior to infection. Maximal time from infection to transfer was defined as one year. The study group was matched by age, number of embryos transferred and day of transfer, to unvaccinated patients, with no history of past infection that underwent FET cycles during the same period. Demographics and cycle characteristics were recorded. Clinical and ongoing pregnancy rates were compared, with further stratification by time from infection.Main results and the role of chanceClinical pregnancy rates were 29.3% and 48.8% for the recovered and control patients respectively (p = 0.070). Ongoing pregnancy rates were 26.6% vs. 43.4% (p = 0.093). Mean age at ovum pickup (30.72 vs. 30.69; p = 0.929) and at transfer (31.56 vs. 31.58; p = 0.966) was similar between groups, as were the demographic characteristics and previous retrievals and transfers. The predominant transfer protocol used was different between groups with higher rates of natural cycle (NC) protocol in the COVID group (61% vs. 33.3%; p = 0.013. All other cycle characteristics including endometrial width, number of embryos transferred, day of embryo transfer and embryo grade were similar. Stratification by time from COVID-19 infection to transfer into ≤60 and >60 days revealed a significant difference in pregnancy rates, with recovered women having lower pregnancy rates if infected in proximity to the transfer (20.7% vs. 55.2%; p = 0.006). In a logistic regression model, infection was a significant variable (p = 0.05, OR 0.325, 95% CI 0.106-0.998). Logistic regression applied on the subgroup of women infected in proximity to the transfer, further strengthened the univariate results, with COVID-19 infection remaining a significant parameter (p = 0.005, OR 0.072, 95% CI 0.012-0.450).Limitations, reasons for cautionA retrospective study, with a limited sample size, but nevertheless our results showed significant differences. Wider implications of the findingsFurther studies with larger groups are warranted to support these findings. Pending further information, in cases of FET cycles with limited numbers of embryos (advanced age, embryo donation, fertility preservation, embryos following sperm extraction), postponing embryo transfer for at least 60 days following recovery might be considered, if feasible.Trial registration numberHMC-0010-21

Effects of Viral Infection on Endothelial Activation and Barrier Function

Endothelial cells (ECs) are in the inner layer of blood vessels, and it controls the transportation of nutrition and essential molecules from the extracellular matrix to the intracellular space making a homeostasis environment. Vascular endothelium can be disrupted with viruses, which are among the main reasons for epidemic and pandemic outbreaks, and it leads to health issues such as cardiovascular‐related diseases. Wide range of viruses can potentially target the endothelium including Dengue virus estimated to infect 390 million people per year. Zika virus leads to pregnancy complications such as preterm birth and miscarriage. Tick‐borne encephalic damaged the central nervous system and, Hantavirus has a mortality rate of 38% through hantavirus pulmonary syndrome. Reviewing these several diseases, including SARS‐CoV‐2, has given an in‐depth look at what the endothelial cells are going through when these viruses are infecting the host bodies. Following the virus infection, ECs are going through activation mode, which is accompanied with glycocalyx degradation, plasma leakage, phosphorylation of P120, and cadherin, increased proinflammatory responses and, disruption of barrier integrity.The SARS‐CoV‐2 pandemic has taken a global toll; With a total of 362 million cases, there are 5.63 million deaths occurring. With the usage of immunofluorescence and vascular permeability assay, we monitor how Human Umbilical Vascular Endothelial Cells (HUVEC) and Human Lung Microvascular Endothelial Cells (HLMVEC) are impacted when treated with UV‐inactivated & heat‐inactivated SARS‐CoV‐2, and tumor necrosis factor (TNF)‐α. TNF‐α is an inflammatory cytokine prominent during inflammation and its known to increase the permeability of endothelium. Like the TNF‐α, both cells treated with UV‐inactivated and heat‐inactivated SARS‐CoV2 demonstrated boosted permeability. With the considerable effect of SARS‐CoV2 on the permeability of ECs, it is essential to understand the mechanisms and pathways behind the boosted leak, including the impact of the virus on the expression of adhesion molecules like platelet endothelial cell adhesion molecule (PECAM‐1). One can see in the images of HUVEC and HLMVEC that SARS‐CoV‐2 diminish the localization of PECAM‐1. On a non‐treated negative control, cells are spaced evenly and are close to another since their junctions are not targeted. Once the cells are treated with either heat‐inactivated or UV‐inactivated SARS‐CoV‐2, PECAM‐1 localization is disrupted, which can be seen from the space between cells since the PECAM‐1 has been altered and is no longer holding the cells together. From those exact images, one can detect the enlarged and irregular shapes of nucleuses and change in morphology of these cells since the SARS‐CoV‐2 is not only altering the PECAM‐1 complex but it can also modify various proteins and mRNAs. By combining information of various viruses and knowledge from our studies, we can understand the mechanisms of ECs and take measurements to protect ECs from viruses. In future experiments, we will detect if the PECAM‐1 expression is lowered when treated with SARS‐CoV‐2 and TNF‐α or if PECAM‐1 is internalized in the cell. Moreover, we can do mRNA and immunoblotting analysis to elaborate the changes in protein pathways as a consequence of COVID‐19.

Comparison of the levels of neopterin, CRP, and IL-6 in patients infected with and without SARS-CoV-2

BackgroundNeopterin (NP) is a biomarker for activated cellular immunity and is elevated in diseases including viral and bacterial infections, autoimmune diseases, and cancer. However, the clinical assessment of neopterin has not been used for these disorders because the physiological significance of measuring NP is obscure. It would be important to compare the NP profiles with those of other inflammation markers especially in relatively early phase of patients to reveal the significance of NP measurements in pathological states. MethodsPlasma NP, biopterin, CRP, and IL-6 levels were measured in 46 patients with Coronavirus Disease 2019 (COVID-19) and 23 patients with non-COVID-19 disorders. The correlations between these markers were analyzed in the COVID-19 and non-COVID-19 patients independently. ResultsThe NP levels were significantly higher in the COVID-19 patients than in the non-COVID-19 patients, while biopterin, CRP and IL-6 were not changed significantly. The NP levels were found to show a weak negative correlation against the days after onset in the COVID-19 patients (rs = –0.348, p = 0.0192), suggesting that the elevation of NP would be an early event of viral infection. Correlations between NP and CRP, or between NP and IL-6 in COVID-19 patients were weaker than that between CRP and IL-6. ConclusionsThe elevation of NP levels was supposed to be distinct from those of CRP and IL-6 in relatively early and mild COVID-19 patients. Our data suggest that NP is produced at the early phase of infection by different signaling pathways and/or cells from those of CRP and IL-6. Further study on the signaling pathway to induce NP is expected.

Microtubule depolymerization limits porcine betacoronavirus PHEV replication

Porcine hemagglutinating encephalomyelitis virus (PHEV) is a typical neurotropic betacoronavirus causing digestive disease and/or neurological dysfunction in neonatal pigs. Actin filaments have been identified to implicate in PHEV invasion, but the effects of viral infection on microtubules (MTs) cytoskeleton are unknown. Here, we observed that PHEV infection induced MT depolymerization and was accompanied by the disappearance of microtubule organizing centers. Depolymerization of MTs induced by nocodazole significantly inhibited viral RNA replication, but over-polymerization of MTs induced by paclitaxel did not substantially affect PHEV infection. The expression of histone deacetylase 6 (HDAC6), an important regulator of MT acetylation, progressively increased during PHEV infection. Tramstatin A could alter HDAC6 deacetylase activity to enhance the acetylation of the substrate α-tubulin and MT polymerization, but does not increase PHEV proliferation. These findings suggest that PHEV could subvert host MT cytoskeleton to facilitate infection, and that MT depolymerization negatively affects viral replication independently of HDAC6 activity.