BackgroundA spectrum of adverse events overlapping with Post-acute Sequelae of SARS-CoV-2 infection (PASC) occurs in some patients following SARS-CoV-2 vaccination including small fiber neuropathy (SFN) and cognitive symptoms.AimsAccruing information regarding disease course and immune response imbalances in these patients.MethodsWe studied 71 previously healthy patients with neurological symptoms following SARS-CoV-vaccination. All had negative neurological workup for central/peripheral involvement (MR, EMG/EN). Cutaneous biopsy (21pts.) and peripheral blood sampling (20pts) were performed for anti-idiotype Ab analysis (ACE-2,NRP-1) (ELISA, IF) and for Flowcytometric analysis.ResultsParesthesia, cognitive impairment and autonomic symptoms agreed with SFN international definition. Comparative differences included abrupt onset, presence of simultaneous diverse paresthesia across multiple body regions frequently affecting the facial and cervical regions (44%) and the trunk (26%), associated to dysautonomia. Median time from vaccination to symptom manifestation was 3 days (mean ± SD: 8.76 ± 17.4 days). Symptom severity was still high (5.9 ± 1.9 mean+SD) at the time of evaluation and sampling, (382 ± 133 days from onset. Reduced small fiber density was observed in 19/21 biopsies. Anti-ACE-2 antibodies in 9/71pts. (12%) and 4/19 (21%) vaccinated HD sera and NRP-1 reactivity in 14/71 (20%) patient and 1/19 (5%) HD sera were not significantly increased. Peripheral NKG2D+CD8+ and NKG2D+DNAM-1+CD4+ T-cells were increased. Circulating inflammatory CD34+ cells were increased and generated in vitro a prevalence of NKG2D+DNAM-1+ T-cells.ConclusionPASC-vac SFN is associated with persistent immune imbalances common to other immune-mediated diseases. Additional effort to identify immune mechanisms unleashing PASC-vac SFN will contribute to modulate future early interventions for these patients and refine vaccine design.

TAS2R38 is the T2R receptor primarily associated with the innate immune response of the respiratory system. It activates a response mediated by nitric oxide (NO), which has been shown to inhibit the replication of SARS-CoV-2. TAS2R38 polymorphisms (SNPs) that decrease receptor functionality contributing to individual differences in susceptibility to airway infections. DNA methylation (DNAm) may affect gene expression influencing disease development, including COVID-19. We analyzed the effect of SARS-CoV-2 on the methylation pattern of TAS2R38 (at cg25481253, a CpG site located in the coding region) during infection and after the cessation of the exposure to the virus, also considering the disease severity and TAS2R38 SNPs. Our results showed a positive relationship between TAS2R38 DNAm levels and disease severity in the COVID-19 patients and a return to a normal state after the infection. In addition, our results showed an association between DNAm level and the TAS2R38 genotype in participants who recovered from the disease. PAV/PAV genotypes showed lower TAS2R38 DNAm levels than heterozygous and AVI homozygous. In conclusion, our results clearly indicate the involvement of TAS2R38 DNAm alteration in COVID-19 severity and suggest a role of the methylation changes at cg25481253 in the regulation of the TAS2R38 expression.

During the COVID-19 pandemic, severe acute respiratory syndrome coronavirus 2 (SC2) infection was confirmed in various animal species demonstrating a wide host range of the virus. Prior studies have shown that the ACE2 protein is the primary receptor used by the virus to gain cellular entry and begin the replication cycle. In previous studies, we demonstrated that human and various bat ACE2 proteins can be utilized by SC2 viruses for entry. Bats are a suspected natural host of SC2 because of genetic homology with other bat coronaviruses. In this work, we demonstrate that expression of ACE2 genes from the common vampire bat (CVB) (Desmodus rotundus) and the pallid bat (PB) (Antrozous pallidus), supports infection and replication of some SC2 viruses in cell culture. Two cell lines were produced, CVB-ACE2 and PB-ACE2, expressing ACE2 from these bat species along with human TMPRSS2, in a model previously established using a non-permissive chicken DF-1 cell line. Results demonstrate that the original Wuhan lineage (WA1) virus and the Delta variant were able to infect and replicate in either of the bat ACE2 cell lines. In contrast, the Lambda and Omicron variant viruses infected both cell lines, but viral titers did not increase following infection. Viral detection using immunofluorescence demonstrated abundant spike (S) protein staining for the WA1 and Delta variants but little signal for the Lambda and Omicron variants. These studies demonstrate that while ACE2 from CVB and PB can be utilized by SC2 viruses to gain entry for infection, later variants (Lambda and Omicron) replicate poorly in these cell lines. These observations suggest more efficient human adaption in later SC2 variants that become less fit for replication in other animal species.

High-affinity and specific binding toward the human angiotensin-converting enzyme 2 (hACE2) receptor by severe acute respiratory syndrome coronavirus (SARS)-related coronaviruses (SARSr-CoVs) remains incompletely understood. We report cryo-electron microscopy structures of eight different S-proteins from SARSr-CoVs found across Asia, Europe, and Africa. These S-proteins all adopt tightly packed, locked, prefusion conformations. These structures enable the classification of SARSr-CoV S-proteins into three types, based on their receptor-binding motif (RBM) structures and ACE2 binding characteristics. Type-2 S-proteins often preferentially bind bat ACE2 (bACE2) over hACE2. We report a structure of a type-2 BtKY72-RBD in complex with bACE2 to understand ACE2 specificity. Structure-guided mutagenesis of BtKY72-RBD reveals that multiple synergistic mutations in four different regions of RBM are required to achieve high-affinity hACE2 binding. Similar RBM changes can also confer hACE2 binding to another type-2 BM48-31 S-protein, which is primarily non-ACE2 binding. These results provide an understanding of how high-affinity hACE2 binding may be acquired by SARSr-CoV S-proteins.

Coronavirus disease 2019 (COVID-19) is caused by a new, highly pathogenic severe-acute-respiratory syndrome coronavirus 2 (SARS-CoV-2) that infects human cells through its transmembrane spike (S) glycoprotein. The receptor-binding domain (RBD) of the S protein interacts with the angiotensin-converting enzyme II (ACE2) receptor of the host cells. Therefore, pharmacological targeting of this interaction might prevent infection or spread of the virus. Here, we performed a virtual screening to identify small molecules that block S-ACE2 interaction. Large compound libraries were filtered for drug-like properties, promiscuity and protein-protein interaction-targeting ability based on their ADME-Tox descriptors and also to exclude pan-assay interfering compounds. A properly designed AI-based virtual screening pipeline was applied to the remaining compounds, comprising approximately 10% of the starting data sets, searching for molecules that could bind to the RBD of the S protein. All molecules were sorted according to their screening score, grouped based on their structure and postfiltered for possible interaction patterns with the ACE2 receptor, yielding 31 hits. These hit molecules were further tested for their inhibitory effect on Spike RBD/ACE2 (19-615) interaction. Six compounds inhibited the S-ACE2 interaction in a dose-dependent manner while two of them also prevented infection of human cells from a pseudotyped virus whose entry is mediated by the S protein of SARS-CoV-2. Of the two compounds, the benzimidazole derivative CKP-22 protected Vero E6 cells from infection with SARS-CoV-2, as well. Subsequent, hit-to-lead optimization of CKP-22 was effected through the synthesis of 29 new derivatives of which compound CKP-25 suppressed the Spike RBD/ACE2 (19-615) interaction, reduced the cytopathic effect of SARS-CoV-2 in Vero E6 cells (IC50 = 3.5 μM) and reduced the viral load in cell culture supernatants. Early in vitro ADME-Tox studies showed that CKP-25 does not possess biodegradation or liver metabolism issues, while isozyme-specific CYP450 experiments revealed that CKP-25 was a weak inhibitor of the CYP450 system. Moreover, CKP-25 does not elicit mutagenic effect on Escherichia coli WP2 uvrA strain. Thus, CKP-25 is considered a lead compound against COVID-19 infection.

Antivirals are effective in reducing hospitalisation and death in mild-to-moderate coronavirus 2019 (COVID-19) patients. We estimated the antiviral uptake of nirmatrelvir/ritonavir and molnupiravir in adult patients with a syndrome coronavirus 2 (SARS-CoV-2) infection during the Emergency Use Authorization (EUA) period in Taiwan. A retrospective cohort study was conducted in Taiwan between January 2022 and December 2022. Patients aged ≥18 years with a SARS-CoV-2 infection were included from the Taipei Medical University Clinical Research Database (TMUCRD) and stratified in three risk groups according to World Health Organization criteria. In total, 96 398 COVID-19 patients (mean age 46.7 ± 17.7 years, 45.8% male) were included. Of these patients 69.8% were classified as low risk, 29.8% as moderate risk, and 0.4% as high risk for progression to severe COVID-19. Nirmatrelvir/ritonavir was prescribed in 5.1% of the COVID-19 patients (low risk = 1.0%, moderate risk = 14.3%, high risk = 17.6%). Molnupiravir was prescribed in 1.9% of the COVID-19 patients (low risk = 0.1%, moderate risk = 5.8%, high risk = 6.9%). Nirmatrelvir/ritonavir and molnupiravir were poorly used in the treatment of adult COVID-19 patients in Taiwan during the pandemic in 2022, especially in moderate-to-high risk groups for progression to severe COVID-19.

In this study, we investigated the differences in clinical biochemical values and mitochondrial mass between schizophrenia patients with and without COVID-19, so as to provide assistance to the treatment and management of COVID-19 positive patients with schizophrenia. We undertook an exploratory, retrospective review of patient data from Dec. 6, 2022, to Jan. 31, 2023. A total of 1696 inpatients with psychosis (921 schizophrenia patients and 775 diagnosed with other mental diseases) during this period were identified. Finally, 60 schizophrenia patients were enrolled in our study, and 20 of them were infected with syndrome coronavirus 2 (SARS-CoV-2). The serum biochemical levels and single-cell mitochondrial mass (SCMM) of the T lymphocytes of all schizophrenia patients were analyzed. The serum levels of aspartate aminotransferase (AST), alkaline phosphatase (ALP), creatinine (Cr) and lactate dehydrogenase (LDH) were significantly higher in schizophrenia patients with COVID-19 (SCZ-C) group. In addition, the SCZ-C group showed lower CD3+, CD3+CD4+ and CD3+CD8+ cell counts and higher SCMM of T lymphocytes compared to SCZ group. Furthermore, positive correlations were found between the T-cell subpopulation counts and positive symptom scores on the Positive and Negative Syndrome Scale (PANSS). Our study findings showed that schizophrenia patients with COVID-19 have a phenotype of mitochondrial damage in T lymphocytes and higher serum levels of AST, ALP, Cr and LDH, which might provide evidence for treating individuals with schizophrenia during subsequent spread of infectious disease.

At present, the major public health challenges caused by novel coronavirus infection have gradually subside. However, a large number of people are still suffering from long-novel coronavirus syndrome or post-novel coronavirus syndrome. The clinical manifestations of long coronavirus syndrome are related to multiple systems, such as respiratory, circulatory, nervous, digestive and musculoskeletal systems, with various long-term persistent symptoms after novel coronavirus infection. At the same time, the infection of the novel coronavirus is an important cause of frailty and sarcopenia in the elderly population. However, at present, the scholars have not paid enough attention to the skeletal muscle weakness caused by the novel coronavirus. Therefore, this paper focuses on the long-novel coronavirus syndrome and sarcopenia to explore the pathological mechanism of skeletal muscle attenuation caused by the SARS-CoV-2 mediated "cytokine storm", mitochondrial damage, hypoxia state and other links,so as to raise the attention of clinical and academic researchers and improve the clinical strategy of frailty and sarcopenia after novel coronavirus infection.

Introduction: Severe Acute Respiratory Syndrome Coronavirus-2 (SARS) was first identified in December 2019 in Wuhan, China. Although the respiratory system is infected in this disease, other tissues are prone to coronavirus attack so that the male reproductive system is another target for the virus causing sexual transmission of coronavirus. This study systematically examined the results of studies conducted on COVID-19 and possible sexual transmission of this virus. Method: This was a systematic review study in which the articles and papers were collected by using some keywords such as COVID-19, Semen, Novel Coronavirus, SARS-COV-2, ACE2, and Male Infertility searching through databases (PubMed, Web of Science, Scopus, Google Scholar) using OR and AND operators from December 2019 to November 2020. Finally, 13 papers as eligible articles were studied. Findings: The collected papers were reviewed, and ultimately 13 papers were entered into this study. According to current studies, the Angiotensin-converting enzyme (ACE2), which is found abundantly in testicles can perform as a cellular receptor for SARS-COV-2. This finding is the foundation of this hypothesis that human testis and semen can be infected by SARS-COV-2. In particular, a study showed that SARS-COV-2 might be detected in semen of patients with COVID-19 while other studies found no viral RNA in testicular biopsy tissue. Furthermore, some studies concluded that this virus, even in the acute phase, could not infect testicles or the male genital system. Accordingly, no evidence confirms that this virus can be transmitted through male genital organs. Conclusion: Although this virus has not been detected in semen fluid and it has not been sexually transmitted, one study found this virus in semen of coronavirus-infected patients and introduced its possible sexual transmission. Therefore, there is a low probability of sexual transmission of coronavirus.

Since December 2019, the world has been grappling with an ongoing global COVID-19 pandemic. Various virus variants have emerged over the past two years, each posing a greater threat than its predecessors. The recent appearance of the omicron variant (B.1.1.529) has raised significant alarm within the field of epidemiology due to its highly contagious nature and rapid transmission rate. The omicron variant possessed mutations in the key receptor-binding domain (RBD) region, the S region, and these modifications have shown a notable impact on the strain's susceptibility to neutralizing antibodies. Developing safe and efficient vaccines to prevent a future severe acute respiratory outbreak of coronavirus syndrome 2 (SARS-CoV-2) is significant. Viral surface spike proteins are ideal targets for vaccines. This study aimed to find a multi-subunit chimeric vaccine. After conducting bioinformatics analysis, the recombinant spike (RS) protein of SARS-CoV-2 was deliberately designed and subsequently produced using E. coli expression systems. The immunogenicity of RS and neutralizing antibody responses were evaluated on immunized BALB/c mice. There was a significant difference in antibody titers between RS-immunized mice and control groups. The endpoint of the serum antibody titer of mice immunized with our chimeric protein was 2.5 times higher than that of the negative control. The chimeric construct could present multiple antigens simultaneously, influentially affecting immunization. Sera from mice vaccinated by RS could recognize the SARS-CoV-2 virus and neutralize antibodies. Our chimeric peptide could bind to antibodies in the serum of patients infected with different serotypes of the SARS-CoV-2 virus, such as alpha, delta, and omicron variants. The results indicated that the RS protein would be a potential novel antigenic candidate for subunit vaccine development and could be used as a useful alternative to generate diagnostic serological tests for SARS-CoV-2 infection.

BackgroundDuring endotracheal intubation, extubation, tracheotomy, and tracheotomy tube replacement, the splashed airway secretions of patients will increase the risk of transmission of SARS-CoV‐2 and many other potential viral and bacterial diseases, such as influenza virus, adenovirus, respiratory syncytial virus, rhinovirus, Middle East respiratory coronavirus syndrome (MERS-CoV), Streptococcus pneumoniae, and Mycobacterium tuberculosis. Therefore, it is necessary to establish a barrier between patients and medical workers to reduce the risk of operators’ infection with potentially pathogenic microorganisms.MethodsWe designed a “safety cap” that can be connected to the opening of an endotracheal tube or tracheotomy tube to reduce the diffusion area of respiratory secretions during the process of endotracheal intubation, extubation and tracheotomy tube replace, so as to reduce the infection risk of medical workers.ResultsThrough a series of hydrodynamic simulation analysis and experiments, we demonstrated that the use of “safety cap” can substantially limit the spatter of airway secretions, so as to improve the hospital sanitation.ConclusionThe “safety cap” can effectively limit the dissemination of patients’ respiratory secretions, thus reducing the risk of potential diseases transmission and may have certain application prospects.

The β-coronavirus family, encompassing Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), Severe Acute Respiratory Syndrome Coronavirus (SARS), and Middle East Respiratory Syndrome Coronavirus (MERS), has triggered pandemics within the last two decades. With the possibility of future pandemics, studying the coronavirus family members is necessary to improve knowledge and treatment. These viruses possess 16 non-structural proteins, many of which play crucial roles in viral replication and in other vital functions. One such vital protein is non-structural protein 10 (nsp10), acting as a pivotal stimulator of nsp14 and nsp16, thereby influencing RNA proofreading and viral RNA cap formation. Studying nsp10 of pathogenic coronaviruses is central to unraveling its multifunctional roles. Our study involves the biochemical and biophysical characterisation of full-length nsp10 from MERS, SARS and SARS-CoV-2. To elucidate their oligomeric state, we employed a combination of Multi-detection Size exclusion chromatography (Multi-detection SEC) with multi-angle static light scattering (MALS) and small angle X-ray scattering (SAXS) techniques. Our findings reveal that full-length nsp10s primarily exist as monomers in solution, while truncated versions tend to oligomerise. SAXS experiments reveal a globular shape for nsp10, a trait conserved in all three coronaviruses, although MERS nsp10, diverges most from SARS and SARS-CoV-2 nsp10s. In summary, unbound nsp10 proteins from SARS, MERS, and SARS-CoV-2 exhibit a globular and predominantly monomeric state in solution.

The study included 38 patients requiring endomyocardial biopsy (EMB) during the post-acute phase of coronavirus infection and a control group including patients requiring EMB prior to the SARS-CoV-2 pandemic. The patients' clinical and laboratory data were analyzed. Histological examination and immunohistochemistry (IHC) of the myocardial tissue was conducted with antibodies to CD3, CD68, HLA-DR, MHC1, C1q, VP1 enteroviruses, spike protein SARS-CoV-2, Ang1, von Willebrand factor (VWF), and VEGF. The morphometric analysis included counting the mean number of inflammatory infiltrate cells per mm2 and evaluating the expression of SARS-CoV-2 spike protein, HLA-DR, MHC1, C1q, Ang1, VWF, and VEGF using a scoring system. If the expression of SARS-CoV-2 spike protein was >3 points, an additional IHC test with antibodies to ACE2, CD16 as well as RT-PCR testing of the myocardial tissue were performed. For two patients, immunofluorescence tests of the myocardial tissue were performed using antibody cocktails to SARS-CoV-2 spike protein/CD16, SARS-CoV-2 spike protein/CD68, CD80/CD163. The statistical data analysis was carried out using the Python programming language and libraries such as NumPy, SciPy, Pandas, and Matplotlib. The study demonstrated a significant increase in the number of CD68+ macrophages in the myocardium of PASC patients compared to patients who did not have a history of COVID-19 (p = 0.014 and p = 0.007 for patients with and without myocarditis, respectively), predominantly due to M2 macrophages. An increase in the number of CD68+ macrophages was more frequently observed in patients with shorter intervals between the most recent positive SARS-CoV-2 PCR test and the time of performing the EMB (r = -0.33 and r = -0.61 for patients with and without myocarditis, respectively). The expression scores of Ang1, VEGF, VWF, and C1q in PASC patients did not significantly differ from those in EMB samples taken before 2019. The myocardium of PASC patients demonstrated a significant increase in the number of CD68+ macrophages and a decrease in the expression of markers associated with angiopathy. No evidence of coronavirus-associated myocarditis was observed in any PASC patient.

Vaccination status of COVID-19 patients followed up in the ICU in a country with heterologous vaccination policy: A multicenter national study in Turkey

Community-Acquired Pneumonia (CAP) represents one of the first causes of hospitalization and death in the elderly all over the world and weighs heavily on public health system. Since the beginning of the COVID-19 (CoronaVirus Disease-19) pandemic, everybody’s behavior was forced to change, as the result of a global lockdown strategy and the obligation of using personal protection equipment (PPE). We aimed to evaluate how the mitigation strategies adopted to fight SARS-CoV-2 (Severe Acute Respiratory Coronavirus Syndrome 2) infection have influenced hospitalizations due to CAP in two different Local Health Boards (LHBs) of central Italy. We considered two main periods of observation: before and after the national start of lockdown, in two Abruzzo’s LHBs. We analyzed 19,558 hospital discharge records of bacterial and viral CAP. Excluding SARS-CoV2 infection, a significant decrease in CAP hospitalizations was observed. Through the analysis of Diagnosis Related Group (DRG) values, we highlighted a significant saving of founds for the Regional Health Service. The enactment of social distancing measures to contain COVID-19 spread, brought down admissions for bacterial and viral pneumonia. Our study emphasizes that costs for hospitalizations due to CAP could be drastically reduced by mask wearing and social distancing.

Previous analyses on sex differences in case fatality rates at population-level data had limited adjustment for key patient clinical characteristics thought to be associated with coronavirus disease 2019 (COVID-19) outcomes. We aimed to estimate the risk of specific organ dysfunctions and mortality in women and men. This retrospective cross-sectional study included 17 hospitals within 5 European countries participating in the International Survey of Acute Coronavirus Syndromes COVID-19 (NCT05188612). Participants were individuals hospitalized with positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from March 2020 to February 2022. Risk-adjusted ratios (RRs) of in-hospital mortality, acute respiratory failure (ARF), acute heart failure (AHF), and acute kidney injury (AKI) were calculated for women vs. men. Estimates were evaluated by inverse probability weighting and logistic regression models. The overall care cohort included 4499 patients with COVID-19-associated hospitalizations. Of these, 1524 (33.9%) were admitted to intensive care unit (ICU), and 1117 (24.8%) died during hospitalization. Compared with men, women were less likely to be admitted to ICU [RR: 0.80; 95% confidence interval (CI): 0.71-0.91]. In general wards (GWs) and ICU cohorts, the adjusted women-to-men RRs for in-hospital mortality were of 1.13 (95% CI: 0.90-1.42) and 0.86 (95% CI: 0.70-1.05; pinteraction = 0.04). Development of AHF, AKI, and ARF was associated with increased mortality risk (odds ratios: 2.27, 95% CI: 1.73-2.98; 3.85, 95% CI: 3.21-4.63; and 3.95, 95% CI: 3.04-5.14, respectively). The adjusted RRs for AKI and ARF were comparable among women and men regardless of intensity of care. In contrast, female sex was associated with higher odds for AHF in GW, but not in ICU (RRs: 1.25; 95% CI: 0.94-1.67 vs. 0.83; 95% CI: 0.59-1.16, pinteraction = 0.04). Women in GW were at increased risk of AHF and in-hospital mortality for COVID-19 compared with men. For patients receiving ICU care, fatal complications including AHF and mortality appeared to be independent of sex. Equitable access to COVID-19 ICU care is needed to minimize the unfavourable outcome of women presenting with COVID-19-related complications.

To investigate respiratory virus infections in diarrhea cases and identify the risk of respiratory virus transmission through feces. Fecal specimens were collected from diarrhea cases in enteric disease clinics in Beijing, China, from 2019 to 2020. Cases that tested negative for norovirus, rotavirus, sapovirus, astrovirus, and enteric adenovirus were included in the study. Real-time RT-PCR was used to detect 16 groups of respiratory viruses, and the major viruses were genotyped. Viruses isolation and digestion of clinical specimens and nucleic acid by artificial gastric acid or artificial bile/pancreatic juice were used to evaluate the risk of respiratory virus transmission through feces. A total of 558 specimens were collected and 47 (8.42%) specimens were detected positive, 40 (13.33%, 40/300) in 2019, and 7 (2.71%, 7/258) in 2020, including 20 (3.58%) for human rhinovirus (HRV), 13 (2.32%) for Bocavirus (BoV), 6 (1.08%) for parainfluenza virus I (PIV), 4 (0.72%) for coronavirus (CoV) OC43, 3 (0.54%) for respiratory syncytial virus (RSV) A, and 1 (0.18%) for both BoV and CoV OC43. Syndrome coronavirus 2 (SARS-CoV-2) and other viruses were not detected in this study. Eight genotypes were identified in the 13 HRV specimens. BoVs 1 and 2 were identified in nine BoV specimens. HRV infectious virions were successfully isolated from 2 clinical specimens and clinical specimens of HRV, RSV, PIV, and CoV could not be detected after 4 h of digestion and their nucleic acid could not be detected after 2 h of digestion by artificial gastric acid or artificial bile/pancreatic juice. There may be a risk of respiratory virus transmission from diarrhea cases, and interventions against SARS-COV-2 epidemics are also effective for other respiratory viruses.

Studies suggest infants may be at increased risk of severe coronavirus disease 2019 (COVID-19) relative to older children, but few data exist regarding the incidence of COVID-19 episodes and associated risk factors. We estimate incidence rates and describe characteristics associated with medically attended COVID-19 episodes among infants younger than 6 months of age. We analyzed electronic medical record data from a cohort of infants born March 1, 2020-February 28, 2021. Data from 3 health care delivery systems included demographic characteristics, maternal and infant outpatient visit and hospitalization diagnoses and severe acute respiratory syndrome coronavirus syndrome 2 (SARS-CoV-2) test results. Medically attended COVID-19 episodes were defined by positive SARS-CoV-2 clinical tests and/or COVID-19 diagnosis codes during medical care visits. Unadjusted and site-adjusted incidence rates by infant month of age, low and high SARS-CoV-2 circulation periods and maternal COVID-19 diagnosis were calculated. Among 18,192 infants <6 months of age whose mothers received prenatal care within the 3 systems, 173 (1.0%) had medically attended COVID-19 episodes. Incidence rates were highest among infants under 1 month of age (2.0 per 1000 person-weeks) and 1 month (2.0 per 1000 person-weeks) compared with older infants. Incidence rates were also higher for infants born to women with postpartum COVID-19 compared with women without known COVID-19 and women diagnosed with COVID-19 during pregnancy. Infants of women with postpartum COVID-19 had a higher risk of medically attended COVID-19 than infants born to mothers who were diagnosed during pregnancy or never diagnosed underscoring the importance of COVID-19 prevention measures for their household members and caregivers to prevent infections in infants.

Purpose We investigated plasma angiotensin-converting enzyme 2 (ACE2) concentration in a population sample and the ACE2 expression quantitated with the diaminobenzidine mean intensity in the lung tissue in patients who underwent lung surgery. Materials and methods The study participants were recruited from a residential area in the suburb of Shanghai for the plasma ACE2 concentration study (n = 503) and the lung tissue samples were randomly selected from the storage in Ruijin Hospital (80 men and 78 age-matched women). Results In analyses adjusted for covariables, men had a significantly higher plasma ACE2 concentration (1.21 vs. 0.98 ng/mL, p = 0.027) and the mean intensity of ACE2 in the lung tissue (55.1 vs. 53.9 a.u., p = 0.037) than women. With age increasing, plasma ACE2 concentration decreased (p = 0.001), while the mean intensity of ACE2 in the lung tissue tended to increase (p = 0.087). Plasma ACE2 concentration was higher in hypertension than normotension, especially treated hypertension (1.23 vs. 0.98 ng/mL, p = 0.029 vs. normotension), with no significant difference between users of RAS inhibitors and other classes of antihypertensive drugs (p = 0.64). There was no significance of the mean intensity of ACE2 in the lung tissue between patients taking and those not taking RAS inhibitors (p = 0.14). Neither plasma ACE2 concentration nor the mean intensity of ACE2 in the lung tissue differed between normoglycemia and diabetes (p ≥ 0.20). Conclusion ACE2 in the plasma and lung tissue showed divergent changes according to several major characteristics of patients.

The novel coronavirus (COVID-19) produced severe acute respiratory coronavirus syndrome (SARS-CoV-2; formerly known as 2019-nCoV) and has mild to fatal symptoms. This study aimed to investigate the different blood markers in confirmed positive COVID-19 individuals and see how they associated with the severity of the condition. A cross-sectional study was conducted from September 2020 to March 2021 on seventy-six (20 female and 56 male) Iraqi patients unvaccinated against COVID-19. The mean age of the study subjects was (47.00±13.31; 43.86±14.27) for males and females, respectively. 68.42% of the cases with mild illness, 14.47% with moderate illness, and 17.10% were severely ill. The severity of COVID-19 was assessed by several hematological parameters, including white blood cell (WBC) count, derived indicators such as neutrophils to lymphocyte ratio (NLR) and IL6, C-reactive protein (CRP), D-dimer, and S-ferritin. The results showed that lymphocyte count was lower in severely ill patients compared to patients with mild and moderate symptoms, with a significant difference between the three groups (2.274.83). Additionally, the NLR results showed a significant rise (11.56±1.23) in severe COVID-19. The results of the present study indicated that serum levels of IL6, CRP, and S-ferritin revealed significant differences (41.20±6.23 pg/ml), (50.66±12.55 mg/l), and (454.60±95.69 ng/ml) at (P≤0.05) in sever ill compared with mild and moderately ill patients respectively. The results indicated a highly significant positive correlation between IL6 and severity of COVID-19 infection at P<0.01. Furthermore, a positive connection is seen in Neutrophil, CRP, and NLR (0.229, 0.264, and 0.277) at (P≤0.05) respectively.