Long-Term Taste and Smell Outcomes After COVID-19.

Importance: Self-report surveys suggest that long-lasting taste deficits may occur after SARS-CoV-2 infection, influencing nutrition, safety, and quality of life. However, self-reports of taste dysfunction are inaccurate, commonly reflecting deficits due to olfactory not taste system pathology; hence, quantitative testing is needed to verify the association of post-COVID-19 condition with taste function. Objective: To use well-validated self-administered psychophysical tests to investigate the association of COVID-19 with long-term outcomes in taste and smell function. Design, Setting, and Participants: This nationwide cross-sectional study included individuals with and without a prior history of COVID-19 recruited from February 2020 to August 2023 from a social media website (Reddit) and bulletin board advertisements. In the COVID-19 cohort, there was a mean of 395 days (95% CI, 363-425 days) between diagnosis and testing. Exposure: History of COVID-19. Main Outcomes and Measures: The 53-item Waterless Empirical Taste Test (WETT) and 40-item University of Pennsylvania Smell Identification Test (UPSIT) were used to assess taste and smell function. Total WETT and UPSIT scores and WETT subtest scores of sucrose, citric acid, sodium chloride, caffeine, and monosodium glutamate were assessed for groups with and without a COVID-19 history. The association of COVID-19 with taste and smell outcomes was assessed using analysis of covariance, χ2, and Fisher exact probability tests. Results: Tests were completed by 340 individuals with prior COVID-19 (128 males [37.6%] and 212 females [62.4%]; mean [SD] age, 39.04 [14.35] years) and 434 individuals with no such history (154 males [35.5%] and 280 females [64.5%]; mean (SD) age, 39.99 [15.61] years). Taste scores did not differ between individuals with and without previous COVID-19 (total WETT age- and sex-adjusted mean score, 33.41 [95% CI, 32.37-34.45] vs 33.46 [95% CI, 32.54-34.38]; P = .94). In contrast, UPSIT scores were lower in the group with previous COVID-19 than the group without previous COVID-19 (mean score, 34.39 [95% CI, 33.86-34.92] vs 35.86 [95% CI, 35.39-36.33]; P < .001]); 103 individuals with prior COVID-19 (30.3%) and 91 individuals without prior COVID-19 (21.0%) had some degree of dysfunction (odds ratio, 1.64 [95% CI, 1.18-2.27]). The SARS-CoV-2 variant present at the time of infection was associated with smell outcomes; individuals with original untyped and Alpha variant infections exhibited more loss than those with other variant infections; for example, total to severe loss occurred in 10 of 42 individuals with Alpha variant infections (23.8%) and 7 of 52 individuals with original variant infections (13.5%) compared with 12 of 434 individuals with no COVID-19 history (2.8%) (P < .001 for all). Conclusions and Relevance: In this study, taste dysfunction as measured objectively was absent 1 year after exposure to COVID-19 while some smell loss remained in nearly one-third of individuals with this exposure, likely explaining taste complaints of many individuals with post-COVID-19 condition. Infection with earlier untyped and Alpha variants was associated with the greatest degree of smell loss.

HSPA5 Promotes Attachment and Internalization of Porcine Epidemic Diarrhea Virus through Interaction with the Spike Protein and the Endo-/Lysosomal Pathway.

Porcine epidemic diarrhea virus (PEDV) has caused huge economic losses to the global pig industry. The swine enteric coronavirus spike (S) protein recognizes various cell surface molecules to regulate viral infection. In this study, we identified 211 host membrane proteins related to the S1 protein by pulldown combined with liquid-chromatography tandem mass spectrometry (LC-MS/MS) analysis. Among these, heat shock protein family A member 5 (HSPA5) was identified through screening as having a specific interaction with the PEDV S protein, and positive regulation of PEDV infection was validated by knockdown and overexpression tests. Further studies verified the role of HSPA5 in viral attachment and internalization. In addition, we found that HSPA5 interacts with S proteins through its nucleotide-binding structural domain (NBD) and that polyclonal antibodies can block viral infection. In detail, HSPA5 was found to be involved in viral trafficking via the endo-/lysosomal pathway. Inhibition of HSPA5 activity during internalization would reduce the subcellular colocalization of PEDV with lysosomes in the endo-/lysosomal pathway. Together, these findings show that HSPA5 is a novel PEDV potential target for the creation of therapeutic drugs. IMPORTANCE PEDV infection causes severe piglet mortality and threatens the global pig industry. However, the complex invasion mechanism of PEDV makes its prevention and control difficult. Here, we determined that HSPA5 is a novel target for PEDV which interacts with its S protein and is involved in viral attachment and internalization, influencing its transport via the endo-/lysosomal pathway. Our work extends knowledge about the relationship between the PEDV S and host proteins and provides a new therapeutic target against PEDV infection.

La cardiología nuclear en la pandemia COVID-19 / Nuclear Cardiology in the COVID-19 pandemic

La infección por SARS-CoV-2 tiene una relación muy importante con la patología cardiovascular. Desde el inicio de la pandemia se objetivó una relación estrecha entre la comorbilidad cardiovascular y un peor pronóstico de los pacientes COVID-19. El estudio de la fisiopatología de la infección por SARS-CoV-2 y la enfermedad cardiovascular sugieren varias hipótesis concomitantes: el daño miocárdico directo por el virus, la hipoxemia secundaria a la insuficiencia respiratoria, la respuesta inflamatoria a la infección y/o los fenómenos tromboembólicos. El daño cardiovascular se puede manifestar en la fase aguda de la infección con cuadros de infarto agudo de miocardio, miocarditis, arritmias…, durante esta fase los procedimientos de Cardiología Nuclear no han tenido un papel determinante en el diagnóstico y manejo de estos pacientes. En cambio, en la fase subaguda de la infección y en el síndrome del COVID post-agudo la Cardiología Nuclear parece ofrecer luz a lo que sucede en el sistema cardiovascular en esta fase de la enfermedad. La pandemia de la COVID-19 ha representado un gran reto para los sistemas de salud constatándose una reducción importante de pruebas diagnósticas no urgentes con el objetivo de disminuir el riesgo de transmisión a pacientes y personal sanitario. La Cardiología Nuclear no ha sido una excepción. Además de la priorización de pruebas urgentes/preferentes y las medidas generales de screening, higiene y distancia, los principales organismos y sociedades científicas de Medicina Nuclear y Cardiología Nuclear han elaborado recomendaciones y guías para su práctica segura introduciendo notables cambios en los protocolos SPECT de perfusión miocárdica (AU)

SARS-CoV-2 infection has a very important relationship with cardiovascular disease. Since the beginning of the pandemic, a close relationship has been observed between cardiovascular comorbidity and a worse prognosis in COVID-19 patients. The study of the pathophysiology of SARS-CoV-2 infection and cardiovascular disease suggests several concomitant hypotheses: direct myocardial damage by the virus, hypoxemia secondary to respiratory failure, inflammatory response to infection and/or thromboembolic phenomena. Cardiovascular damage can manifest in the acute phase of infection with acute myocardial infarction, myocarditis, arrhythmias..., during this phase Nuclear Cardiology procedures have not played a determining role in the diagnosis and management of these patients. On the other hand, in the subacute phase of the infection and in the post-acute COVID syndrome, Nuclear Cardiology seems to shed light on what happens in the cardiovascular system in this phase of the disease. The COVID-19 pandemic has represented a great challenge for health systems, with a significant reduction in non-urgent diagnostic procedures with the aim of reducing the risk of transmission to patients and health personnel. Nuclear Cardiology has not been an exception. In addition to the prioritization of urgent/non-deferrable procedures and general screening, hygiene and distance measures, the main organizations and scientific societies of Nuclear Medicine and Nuclear Cardiology released recommendations and guidelines for safe practice, introducing significant changes in myocardial perfusion SPECT protocol (AU)

Genome-Wide CRISPR/Cas9 Screen Reveals a Role for SLC35A1 in the Adsorption of Porcine Deltacoronavirus.

Porcine deltacoronavirus (PDCoV), an emerging enteropathogenic coronavirus, not only causes diarrhea in piglets but also possesses the potential to infect humans. To better understand host-virus genetic dependencies and find potential therapeutic targets for PDCoV, we used a porcine single-guide RNA (sgRNA) lentivirus library to screen host factors related to PDCoV infection in LLC-PK1 cells. The solute carrier family 35 member A1 (SLC35A1), a key molecule in the sialic acid (SA) synthesis pathway, was identified as a host factor required for PDCoV infection. A knockout of SLC35A1 caused decreases in the amounts of cell surface sialic acid (SA) and viral adsorption; meanwhile, trypsin promoted the use of SA in PDCoV infection. By constructing and assessing a series of recombinant PDCoV strains with the deletion or mutation of possible critical domain or amino acid residues for SA binding in the S1 N-terminal domain, we found that S T182 might be a PDCoV SA-binding site. However, the double knockout of SLC35A1 and amino peptidase N (APN) could not block PDCoV infection completely. Additionally, we found that different swine enteric coronaviruses, including transmissible gastroenteritis coronavirus, porcine epidemic diarrhea virus, and swine acute diarrhea syndrome coronavirus, are differentially dependent on SA. Overall, our study uncovered a collection of host factors that can be exploited as drug targets against PDCoV infection and deepened our understanding of the relationship between PDCoV and SA. IMPORTANCE Identifying the host factors required for replication will be helpful to uncover the pathogenesis mechanisms and develop antivirals against the emerging coronavirus porcine deltacoronavirus (PDCoV). Herein, we performed a genome-wide clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 knockout screen, the results of which revealed that the solute carrier family 35 member A1 (SLC35A1) is a host factor required for PDCoV infection that acts by regulating cell surface sialic acid (SA). We also identified the T182 site in the N-terminal domain of PDCoV S1 subunit as being associated with the SA-binding site and found that trypsin promotes the use of cell surface SA by PDCoV. Furthermore, different swine enteric coronaviruses use SLC35A1 differently for infection. This is the first study to screen host factors required for PDCoV replication using a genome-wide CRISPR-Cas9 functional knockout, thereby providing clues for developing antiviral drugs against PDCoV infection.

Long-Term Expanding Porcine Airway Organoids Provide Insights into the Pathogenesis and Innate Immunity of Porcine Respiratory Coronavirus Infection.

Respiratory coronaviruses cause serious health threats to humans and animals. Porcine respiratory coronavirus (PRCoV), a natural transmissible gastroenteritis virus (TGEV) mutant with partial spike deletion, causes mild respiratory disease and is an interesting animal respiratory coronavirus model for human respiratory coronaviruses. However, the absence of robust ex vivo models of porcine airway epithelium hinders an understanding of the pathogenesis of PRCoV infection. Here, we generated long-term porcine airway organoids (AOs) derived from basal epithelial cells, which recapitulate the in vivo airway complicated epithelial cellularity. Both 3D and 2D AOs are permissive for PRCoV infection. Unlike TGEV, which established successful infection in both AOs and intestinal organoids, PRCoV was strongly amplified only in AOs, not intestinal organoids. Furthermore, PRCoV infection in AOs mounted vigorous early type I and III interferon (IFN) responses and upregulated the expression of overzealous inflammatory genes, including pattern recognition receptors (PRRs) and proinflammatory cytokines. Collectively, these data demonstrate that stem-derived porcine AOs can serve as a promising disease model for PRCoV infection and provide a valuable tool to study porcine respiratory infection. IMPORTANCE Porcine respiratory CoV (PRCoV), a natural mutant of TGEV, shows striking pathogenetic similarities to human respiratory CoV infection and provides an interesting animal model for human respiratory CoVs, including SARS-CoV-2. The lack of an in vitro model recapitulating the complicated cellularity and structure of the porcine respiratory tract is a major roadblock for the study of PRCoV infection. Here, we developed long-term 3D airway organoids (AOs) and further established 2D AO monolayer cultures. The resultant 3D and 2D AOs are permissive for PRCoV infection. Notably, PRCoV mediated pronounced IFN and inflammatory responses in AOs, which recapitulated the inflammatory responses associated with PRCoV in vivo infection. Therefore, porcine AOs can be utilized to characterize the pathogenesis of PRCoV and, more broadly, can serve as a universal platform for porcine respiratory infection.

Host E3 ligase HUWE1 attenuates the proapoptotic activity of the MERS-CoV accessory protein ORF3 by promoting its ubiquitin-dependent degradation.

With the outbreak of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), coronaviruses have begun to attract great attention across the world. Of the known human coronaviruses, however, Middle East respiratory syndrome coronavirus (MERS-CoV) is the most lethal. Coronavirus proteins can be divided into three groups: nonstructural proteins, structural proteins, and accessory proteins. While the number of each of these proteins varies greatly among different coronaviruses, accessory proteins are most closely related to the pathogenicity of the virus. We found for the first time that the ORF3 accessory protein of MERS-CoV, which closely resembles the ORF3a proteins of severe acute respiratory syndrome coronavirus and SARS-CoV-2, has the ability to induce apoptosis in cells in a dose-dependent manner. Through bioinformatics analysis and validation, we revealed that ORF3 is an unstable protein and has a shorter half-life in cells compared to that of severe acute respiratory syndrome coronavirus and SARS-CoV-2 ORF3a proteins. After screening, we identified a host E3 ligase, HUWE1, that specifically induces MERS-CoV ORF3 protein ubiquitination and degradation through the ubiquitin-proteasome system. This results in the diminished ability of ORF3 to induce apoptosis, which might partially explain the lower spread of MERS-CoV compared to other coronaviruses. In summary, this study reveals a pathological function of MERS-CoV ORF3 protein and identifies a potential host antiviral protein, HUWE1, with an ability to antagonize MERS-CoV pathogenesis by inducing ORF3 degradation, thus enriching our knowledge of the pathogenesis of MERS-CoV and suggesting new targets and strategies for clinical development of drugs for MERS-CoV treatment.

Pathogenicity of the Canadian Delmarva (DMV/1639) Infectious Bronchitis Virus (IBV) on Female Reproductive Tract of Chickens.

Infectious bronchitis virus (IBV) infection causes significant economic losses to various sectors of the poultry industry worldwide. Over the past few years, the incidence of false layer syndrome in Eastern Canadian layer flocks has been associated with the increased prevalence of the IBV Delmarva (DMV)/1639 strain. In this study, 1-day-old specific-pathogen-free (SPF) hens were infected with the Canadian DMV/1639 strain and observed until 16 weeks of age in order to determine if the IBV DMV/1639 strain is causing false layer syndrome. Early after infection, the virus showed a wide tissue distribution with characteristic gross and histopathological lesions in the respiratory tract and kidney. Around 60-70% of the infected hens demonstrated continuous cloacal viral shedding until the end of the experiment (at 16 weeks) which was associated with high IBV genome loads detected in the cecal tonsils. The experiment confirmed the field observations that the Canadian DMV/1639 strain is highly pathogenic to the female reproductive tract causing marked cystic lesions in the oviduct. Moreover, significant histopathological damage was observed in the ovary. Our study provides a detailed description of the pathological consequences of the IBV DMV/1639 strain circulating in an important poultry production sector.

Decreased NHE3 activity in intestinal epithelial cells in TGEV and PEDV-induced piglet diarrhea.

Transmissible gastroenteritis (TGE) and porcine epidemic diarrhea (PED) are highly transmissible intestinal infections caused by transmissible gastroenteritis virus (TGEV) and porcine epidemic diarrhea virus (PEDV), respectively. They are clinically associated with vomiting, diarrhea, and dehydration in piglets. An imbalance in Na+ uptake by intestinal epithelial cells causes TGEV/PEDV-induced diarrhea. However, the mechanism by which TGEV/PEDV-infection in piglets causes Na+ imbalance diarrhea has not been elucidated. In the present study, we demonstrated that specific inhibition of NHE3 activity caused small intestinal bulging, intestinal wall thinning and severe diarrhea in piglets, consistent with the signs of TGEV/PEDV infection. This study further elucidated the role of NHE3 in TGEV/PEDV-induced diarrhea. In this study, small intestinal epithelial cells (IPEC-J2) were used as a model of infection. The results showed that TGEV/PEDV infection reduced NHE3 activity and Na+ uptake in IPEC-J2 cells. Further studies revealed that the use of NHE3-specific inhibitors could reduce the amount of cell membrane NHE3, thereby decreasing Na+ uptake and ultimately leading to diarrhea. Transcriptomic studies performed on obtained jejunal tissues were also consistent with pre-laboratory results. This study will provide a basis for understanding Na+ imbalance diarrhea caused by TGEV/PEDV, as well as for elucidating the diarrheal pathogenesis of other members of α-animal coronaviruses.

Sintomatología y factores de riesgo presentes en la enfermedad por SARS-CoV-2 / Symptomatology and risk factors present in SARS-CoV-2 disease

Objetivo: Analizar la información obtenida de estudios previos acerca del cuadro clínico presente en enfermedad por SARS -CoV-2, así como los factores de riesgo y vulnerabilidad que predisponen a dicha enfermedad, para determinar los más frecuentes en interés de guiar al buen diagnóstico y tratamiento de la misma. Método: Revisión sistemática utilizando la internet y motores de búsqueda como Google Scholar y PubMed. Las fuentes revisadas se encuentran publicadas en revistas en línea tales como Elsevier, Jama, SciELO, Science Direct, entre otras. Se incluyeron documentos por la Secretaría de Salud de México, y la Organización Mundial de la Salud. Resultados: Se observó que la sintomatología del SARS-CoV-2 es variable, encontraron casos asintomáticos. Existe una alta incidencia en distintos síntomas como son: fiebre, tos seca y cansancio. La COVID-19 tiene una letalidad de 10.2% en México. Entre las complicaciones más comunes se encontraron neumonía, insuficiencia cardiaca. Se observaron varios factores de riesgo que pueden llevar a una muerte como desenlace, tales como: HTA, obesidad, ECV, EPOC, cáncer y diabetes. Existen factores de vulnerabilidad como: inadecuado acceso de agua limpia y saneamiento, infraestructura inadecuada, inseguridad alimentaria, entre otros. Conclusiones: El conocimiento de los síntomas más comunes en la enfermedad por SARS-CoV-2 es una herramienta de utilidad clínica para mejorar la atención médica. La presencia de comorbilidades dispone a un agravamiento significativo de la enfermedad, los factores de riesgo y vulnerabilidad apuntan a la necesidad de optimización de actividades en materia de salud pública.(AU)

Objective: To analyze the information obtained from previous studies about the clinical picture present in SARS -CoV-2 disease, as well as the risk and vulnerability factors that predispose to this disease, in order to determine the most frequent ones in the interest of guiding the good diagnosis and treatment of the disease. Method: The reviewed sources are published in online journals such as Elsevier, Jama, SciELO, Science Direct, among others. Also included were documents published by the Mexican Ministry of Health, and the World Health Organization. Results: It was observed that the symptomatology of SARS-CoV-2 is variable, asymptomatic cases were found. There is a high incidence of different symptoms such as: fever, dry cough, tiredness. COVID-19 has a 10.2% lethality in Mexico. Among the most common complications were found, pneumonia, heart failure. Several risk factors were observed that can lead to death as an outcome, such as: ATH, obesity, CVD, COPD, cancer and diabetes. In addition to these risk factors there are vulnerability factors such as: inadequate access to clean water and sanitation, inadequate infrastructure, food insecurity, among other. Conclusions: The knowledge of the most common symptoms of SARS-CoV-2 disease is a clinically useful tool for improving health care. On the other hand, the presence of comorbidities leads to a significant worsening of the disease, risk and vulnerability factors point to the need for optimization of public health activities.(AU)

The Molecular Interplay between Human Coronaviruses and Autophagy.

Coronavirus disease 2019 (COVID-19), caused by a new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has instantaneously emerged as a worldwide pandemic. However, humans encountered other coronaviruses in the past, and they caused a broad range of symptoms, from mild to life-threatening, depending on the virus and immunocompetence of the host. Most human coronaviruses interact with the proteins and/or double-membrane vesicles of autophagy, the membrane trafficking pathway that degrades and recycles the intracellular protein aggregates, organelles, and pathogens, including viruses. However, coronaviruses often neutralize and hijack this pathway to complete their life cycle. In this review, we discuss the interactions of human coronaviruses and autophagy, including recent data from SARS-CoV-2-related studies. Some of these interactions (for example, viral block of the autophagosome-lysosome fusion), while being conserved across multiple coronaviruses, are accomplished via different molecular mechanisms. Therefore, it is important to understand the molecular interplay between human coronaviruses and autophagy for developing efficient therapies against coronaviral diseases.

Middle East Respiratory Syndrome (MERS) Virus-Pathophysiological Axis and the Current Treatment Strategies.

Middle East respiratory syndrome (MERS) is a lethal respiratory disease with its first case reported back in 2012 (Jeddah, Saudi Arabia). It is a novel, single-stranded, positive-sense RNA beta coronavirus (MERS-CoV) that was isolated from a patient who died from a severe respiratory illness. Later, it was found that this patient was infected with MERS. MERS is endemic to countries in the Middle East regions, such as Saudi Arabia, Jordan, Qatar, Oman, Kuwait and the United Arab Emirates. It has been reported that the MERS virus originated from bats and dromedary camels, the natural hosts of MERS-CoV. The transmission of the virus to humans has been thought to be either direct or indirect. Few camel-to-human transmissions were reported earlier. However, the mode of transmission of how the virus affects humans remains unanswered. Moreover, outbreaks in either family-based or hospital-based settings were observed with high mortality rates, especially in individuals who did not receive proper management or those with underlying comorbidities, such as diabetes and renal failure. Since then, there have been numerous reports hypothesising complications in fatal cases of MERS. Over the years, various diagnostic methods, treatment strategies and preventive measures have been strategised in containing the MERS infection. Evidence from multiple sources implicated that no treatment options and vaccines have been developed in specific, for the direct management of MERS-CoV infection. Nevertheless, there are supportive measures outlined in response to symptom-related management. Health authorities should stress more on infection and prevention control measures, to ensure that MERS remains as a low-level threat to public health.

Obesidad: factor de riesgo para psoriasis y COVID-19 / Obesity — A Risk Factor for Psoriasis and COVID-19

La obesidad es un importante problema sanitario y su asociación a la psoriasis es bien conocida y ha sido ampliamente descrita. Recientemente, su relevancia en relación con la COVID-19, enfermedad causada por el betacoronavirus SARS-CoV-2, se ha puesto de manifiesto al demostrarse que es un factor de mal pronóstico para estos pacientes. En este trabajo se analiza la relación que puede existir entre obesidad, psoriasis y COVID-19, analizando los nexos fisiopatológicos comunes entre estas entidades y las implicaciones prácticas de esta asociación. Por un lado, el aumento del índice de masa corporal aumenta el riesgo de padecer psoriasis y, además, la obesidad es un factor implicado tanto en el síndrome metabólico, que también está incrementado en pacientes con psoriasis, como en una menor eficacia de los tratamientos. Por otro lado, la obesidad es un factor de riesgo para gravedad de la COVID-19 y para su mortalidad. Además, a nivel pulmonar promueve un estado proinflamatorio y tiene un efecto mecánico desfavorable (AU)

Obesity is a major health problem whose well-known association with psoriasis has been amply described. The importance of obesity as a risk factor for poor prognosis in the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 infection has recently been demonstrated. This review examines a possible relationship between obesity, psoriasis, and COVID-19, analyzing the pathophysiological links and their practical implications. On the one hand, a higher body mass index increases the risk of psoriasis and is also a factor in metabolic syndrome, which is common in patients with psoriasis and has been implicated in reducing the effectiveness of psoriasis treatments. On the other hand, obesity is a risk factor for severe COVID-19 and mortality. Obesity also promotes a proinflammatory state in the lung, where it compromises respiratory mechanics (AU)

Sequence and phylogentic analysis of MERS-CoV in Saudi Arabia, 2012-2019.

BACKGROUND: The Middle East Respiratory Syndrome-related Coronavirus (MERS-CoV) continues to exist in the Middle East sporadically. Thorough investigations of the evolution of human coronaviruses (HCoVs) are urgently required. In the current study, we studied amplified fragments of ORF1a/b, Spike (S) gene, ORF3/4a, and ORF4b of four human MERS-CoV strains for tracking the evolution of MERS-CoV over time. METHODS: RNA isolated from nasopharyngeal aspirate, sputum, and tracheal swabs/aspirates from hospitalized patients with suspected MERS-CoV infection were analyzed for amplification of nine variable genomic fragments. Sequence comparisons were done using different bioinformatics tools available. RESULTS: Several mutations were identified in ORF1a/b, ORF3/4a and ORF4b, with the highest mutation rates in the S gene. Five codons; 4 in ORF1a and 1 in the S gene, were found to be under selective pressure. Characteristic amino acid changes, potentially hosted and year specific were defined across the S protein and in the receptor-binding domain Phylogenetic analysis using S gene sequence revealed clustering of MERS-CoV strains into three main clades, A, B and C with subdivision of with clade B into B1 to B4. CONCLUSIONS: In conclusion, MERS-CoV appears to continuously evolve. It is recommended that the molecular and pathobiological characteristics of future MERS-CoV strains should be analyzed on regular basis to prevent potential future outbreaks at early phases.

SARS-CoV 2 Infection (Covid-19) and Cardiovascular Disease in Africa: Health Care and Socio-Economic Implications.

The current pandemic of SARS-COV 2 infection (Covid-19) is challenging health systems and communities worldwide. At the individual level, the main biological system involved in Covid-19 is the respiratory system. Respiratory complications range from mild flu-like illness symptoms to a fatal respiratory distress syndrome or a severe and fulminant pneumonia. Critically, the presence of a pre-existing cardiovascular disease or its risk factors, such as hypertension or type II diabetes mellitus, increases the chance of having severe complications (including death) if infected by the virus. In addition, the infection can worsen an existing cardiovascular disease or precipitate new ones. This paper presents a contemporary review of cardiovascular complications of Covid-19. It also specifically examines the impact of the disease on those already vulnerable and on the poorly resourced health systems of Africa as well as the potential broader consequences on the socio-economic health of this region.

Telemedicine Strategy for CPAP Titration and Early Follow-up for Sleep Apnea During COVID-19 and Post-Pandemic Future / La estrategia de la telemedicina para la regulación de la CPAP y el seguimiento temprano de la apnea del sueño durante la pandemia de covid-19 y el futuro post-pandémico

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Lung Function sequelae in COVID-19 Patients 3 Months After Hospital Discharge / Secuelas en la función pulmonar de los pacientes con COVID-19 tres meses después del alta hospitalaria

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Fumador, exfumador y COVID-19 / Smoker, Former Smoker and COVID-19

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Low-Level Middle East Respiratory Syndrome Coronavirus among Camel Handlers, Kenya, 2019.

Although seroprevalence of Middle East respiratory coronavirus syndrome is high among camels in Africa, researchers have not detected zoonotic transmission in Kenya. We followed a cohort of 262 camel handlers in Kenya during April 2018-March 2020. We report PCR-confirmed Middle East respiratory coronavirus syndrome in 3 asymptomatic handlers.