Covid19-Sources

Results suggest that vaccines offer less protection against lingering symptoms than expected.

The global spread of Severe Acute Respiratory Syndrome Coronavirus 2. (SARS-CoV-2) and its variant strains, including Alpha, Beta, Gamma, Delta, and now Omicron, pose a significant challenge. With the constant evolution of the virus, Omicron and its subtypes BA.1, BA.2, BA.3, BA.4, and BA.5 have developed the capacity to evade neutralization induced by previous vaccination or infection. This evasion highlights the urgency in discovering new monoclonal antibodies (mAbs) with neutralizing activity, especially broadly neutralizing antibodies (bnAbs), to combat the virus.In the current study, we introduced a fully human neutralizing mAb, CR9, that targets Omicron variants. We demonstrated the mAb’s effectiveness in inhibiting Omicron replication both in vitro and in vivo. Structural analysis using cryo-electron microscopy (cryo-EM) revealed that CR9 binds to an epitope formed by RBD residues, providing a molecular understanding of its neutralization mechanism. Given its potency and specificity, CR9 holds promise as a potential adjunct therapy for treating Omicron infections. Our findings highlight the importance of continuous mAb discovery and characterization in addressing the evolving threat of COVID-19.

Coronavirus disease 2019 (COVID-19) presents a wide spectrum of symptoms, the causes of which remain poorly understood. This study explored the associations between autoantibodies (AABs), particularly those targeting G protein-coupled receptors (GPCRs) and renin‒angiotensin system (RAS) molecules, and the clinical manifestations of COVID-19. Using a cross-sectional analysis of 244 individuals, we applied multivariate analysis of variance, principal component analysis, and multinomial regression to examine the relationships between AAB levels and key symptoms. Significant correlations were identified between specific AABs and symptoms such as fever, muscle aches, anosmia, and dysgeusia. Notably, anti-AGTR1 antibodies, which contribute to endothelial glycocalyx (eGC) degradation, a process reversed by losartan, have emerged as strong predictors of core symptoms. AAB levels increased with symptom accumulation, peaking in patients exhibiting all four key symptoms. These findings highlight the role of AABs, particularly anti-AGTR1 antibodies, in determining symptom severity and suggest their involvement in the pathophysiology of COVID-19, including vascular complications.

We identified seven distinct coronaviruses (CoVs) in bats from Brazil, classified into 229E-related (Alpha-CoV), Nobecovirus, Sarbecovirus, and Merbecovirus (Beta-CoV), including one closely related to MERS-like CoV with 82.8% genome coverage. To accomplish this, we screened 423 oral and rectal swabs from 16 different bat species using molecular assays, RNA sequencing, and evolutionary analysis. Notably, gaps in the spike-encoding gene led us to design new primers and perform Sanger sequencing, which revealed high similarities to MERS-related (MERSr) CoV strains found in humans and camels. Additionally, we identified key residues in the receptor-binding domain (RBD) of the spike protein, suggesting potential interactions with DPP4, the receptor for MERSr-CoV. Our analyses also revealed evidence of recombination involving our laboratory-produced sequences. These findings highlight the extensive genetic diversity of CoVs, the presence of novel viral lineages, and the occurrence of recombination events among bat CoVs circulating in Brazil, underscoring the critical role bats play as reservoirs for emerging viruses and emphasizing the necessity of ongoing surveillance to monitor the public health risks associated with CoV spillover events.

Pulmonary and extrapulmonary manifestations have been reported following infection with SARS-CoV-2, the causative agent of COVID-19. The virus persists in multiple organs due to its tropism for various tissues, including the skeletal system. This study investigates the effects of SARS-CoV-2 infection, including both ancestral and Omicron viral strains, on differentiating mesenchymal stem cells (MSCs), the precursor cells, into osteoblasts. Although both viral strains can productively infect osteoblasts, precursor cell infection remained abortive. Viral exposure during osteoblast differentiation demonstrates that both variants inhibit mineral and organic matrix deposition. This is accompanied by reduced expression of runt-related transcription factor 2 (RUNX2) and increased levels of interleukin-6 (IL-6), a cytokine that negatively regulates osteoblast differentiation. Furthermore, the upregulation of receptor activator of nuclear factor kappa B ligand (RANKL) strongly suggests that the ancestral and Omicron variants may disrupt bone homeostasis by promoting osteoclast differentiation, ultimately leading to the formation of bone-resorbing cells. This process is dependent of spike glycoprotein since its neutralization significantly reduced the effect of infective SARS-CoV-2 and UV-C inactivated virus. This study underscores the capacity of ancestral and Omicron SARS-CoV-2 variants to disrupt osteoblast differentiation, a process essential for preserving the homeostasis and functionality of bone tissue.

Since 2019, SARS-CoV-2 has precipitated an unprecedented global health crisis (1). While many patients infected with the virus exhibit mild to moderate symptoms, including cough, fever, and headache, some progress to severe pneumonia and respiratory failure (1, 2). Severe patients typically experience significant dysfunctional immune responses and cytokine storms, which can progress to acute respiratory distress syndrome (ARDS) (3). The severity of the disease is determined by multiple factors, including individual susceptibility, differences in immunity, and pathogen virulence. As new variants continue to emerge, clinical and experimental results reveal that the pathogenicity of the virus is constantly evolving (4–6). Compared to the wild-type strain, infection with the Alpha and Beta variants results in a higher mortality rate in the K18-hACE2 mouse strain, which is susceptible to SARS-CoV-2 (7). The heightened fusogenicity caused by the P681R mutation in the spike protein of the Delta variant could be a factor contributing to increased severity and unusual symptoms (8). Additionally, the reduced spread of the Omicron variant in lung tissue might be related to its attenuated pathogenicity (9). However, it remains unclear which proteins of SARS-CoV-2 play a decisive role in this process. There is an imperative to understand the internal mechanisms of virus pathogenicity evolution, which is conducive to virus virulence prediction and drug development. Various theories have attempted to explain the pathogenic mechanisms of SARS-CoV-2. Mutations in accessory proteins such as ORF3a and ORF8 can disrupt innate immune signaling, impacting viral pathogenicity (10). The fusogenicity and S1/S2 cleavage efficiency of SARS-CoV-2 may be associated with its pathogenicity (8, 9). Mutations in the Spike protein and NSP6 can reduce replication efficiency in Omicron, thereby weakening its pathogenicity (11). Mutations in the E protein can attenuate its intrinsic toxicity, potentially contributing to reduced pathogenicity (12, 13). Additionally, mutations in NSP4 can inhibit chemokine secretion and reduce host inflammatory responses, thereby attenuating the pathogenicity of the Omicron variant (14). While these studies provide some insights into the pathogenicity changes associated with certain variants, they could not fully explain the evolution of SARS-CoV-2 pathogenicity. For instance, ORF3a is unmutated in both the Alpha and Omicron variants, while the E protein and NSP4 are unmutated in Alpha, Gamma, and Delta variants, suggesting that these proteins do not drive the pathogenicity differences among these variants of concern (VOCs). Mutations in the Spike protein appear closely linked to viral pathogenicity. However, individual Spike protein mutations alone do not replicate the pathogenic profile observed in variant strains (11). Therefore, the pathogenicity of SARS-CoV-2 seems to be the result of multiple virulence factors acting in concert. Systematically understanding the role of SARS-CoV-2 virulence factors and their mutations is essential for elucidating the pathogenic mechanisms. Here, we conduct a thorough review of existing literature to integrate findings from experimental studies, epidemiological data, and clinical research on the subject. We believe that this combined review will allow us to gain deeper insights into the factors driving viral pathogenicity and provide a comprehensive understanding of the mechanisms that differentiate the VOCs in terms of their virulence.

DMZ – FORSCHUNG ¦ Sarah Koller ¦ Seit dem Ausbruch der COVID-19-Pandemie standen Gesundheitssysteme weltweit unter immensem Druck. Das hochansteckende SARS-CoV-2-Virus verbreitete sich schnell und führte zu einer globalen Gesundheitskrise. Während COVID-19 vorwiegend als Atemwegserkrankung bekannt ist, wurde zunehmend klar, dass das Virus auch erhebliche Auswirkungen auf das Herz-Kreislauf-System haben kann. Kardiovaskuläre Risiken bei COVID-19 COVID-19-Patienten haben ein signifikant erhöhtes Risiko, kardiovaskuläre Erkrankungen zu entwickeln. Zu den häufigsten Herzkomplikationen zählen akute Myokardverletzungen, Herzinsuffizienz, Myokarditis, Herzrhythmusstörungen und akute Herzinfarkte. Auch seltenere Krankheitsbilder wie das Takotsubo-Syndrom ("Broken-Heart-Syndrom") und kardiogener Schock wurden im Zusammenhang mit SARS-CoV-2 dokumentiert. Wissenschaftliche Studien haben gezeigt, dass SARS-CoV-2 mehrere Mechanismen nutzt, um das Herz-Kreislauf-System zu schädigen. Das Virus kann akute Koronarsyndrome auslösen, die sowohl mit verengten als auch mit unauffälligen Koronararterien einhergehen. Darüber hinaus wurden Mikrogefäßdysfunktion, Entzündungen der Gefäße (Vaskulitis), endotheliale Schädigungen (Endothelitis) und in-situ-Thrombosen beobachtet. Eine umfassende Meta-Analyse zu kardiovaskulären Komplikationen bei COVID-19 bestätigte diese Befunde. Diagnostik und Therapieansätze Die Diagnostik von kardiovaskulären Komplikationen bei COVID-19 erfordert eine genaue klinische Untersuchung. Symptome wie Brustschmerzen, Atemnot oder Schocksymptome sollten immer auf eine mögliche Herzbeteiligung hin untersucht werden. Wichtige diagnostische Mittel sind Elektrokardiogramme (EKG), Biomarker für Myokardschäden (hsTnT/I, NT-proBNP) und bildgebende Verfahren wie Echokardiografie und CT-Koronarangiografie (CTCA). Diese Methoden sind entscheidend, um zwischen einem Myokardinfarkt und einer Myokarditis zu unterscheiden, insbesondere bei Patienten ohne signifikante Koronarläsionen. Akute Patienten, die mit Symptomen eines Herzinfarkts eingeliefert werden, benötigen häufig eine sofortige interventionelle Therapie. Die primäre perkutane Koronarintervention (PCI) bleibt die Standardbehandlung, auch bei COVID-19-Patienten mit ST-Hebungsinfarkt (STEMI). In Fällen, in denen eine PCI nicht innerhalb von 120 Minuten möglich ist, kann eine Fibrinolyse als Übergangslösung dienen. Allerdings ist dies bei COVID-19-Patienten mit unauffälligen Koronararterien oft nicht indiziert, da keine signifikanten Koronarläsionen vorliegen. Herausforderungen während der Pandemie Die Pandemie führte zu erheblichen Verzögerungen in der Behandlung von Patienten mit akuten Herzerkrankungen. Eine Untersuchung des Journal of the American College of Cardiology zeigte, dass sich sowohl die Zeit bis zum ersten medizinischen Kontakt als auch die Zeit bis zur Durchführung einer PCI während der Pandemie signifikant verlängert haben. Gründe hierfür waren unter anderem die überlasteten Notfallkapazitäten, ein Mangel an Tests und die Sorge des medizinischen Personals vor einer Ansteckung. Diese Verzögerungen hatten schwerwiegende Folgen: In einer Studie, die in JAMA veröffentlicht wurde, konnte gezeigt werden, dass die Mortalität bei STEMI-Patienten während der Pandemie um 27 % höher lag als in der Zeit vor der Pandemie. Langzeitprognose und Forschungsbedarf Patienten mit einer COVID-19-bedingten Myokardverletzung haben ein signifikant höheres Sterblichkeitsrisiko. Besonders ältere Patienten sowie solche mit Vorerkrankungen und starker Entzündungsreaktion sind gefährdet. Darüber hinaus ist die Prognose von Patienten mit Typ-2-Myokardinfarkt, der durch systemische Belastungen wie Sauerstoffmangel und Entzündungen verursacht wird, deutlich schlechter als die von Typ-1-Infarktpatienten. Um die langfristigen Auswirkungen von COVID-19 auf das Herz-Kreislauf-System besser zu verstehen, ist weitere Forschung unerlässlich. Insbesondere die Frage, wie sich die Krankheit langfristig auf die Herzgesundheit auswirkt und welche Präventions- und Behandlungsstrategien optimiert werden können, bedarf intensiver wissenschaftlicher Untersuchung. Mehrere laufende Langzeitstudien in Europa und den USA zielen darauf ab, diese Wissenslücken zu schließen. Fazit COVID-19 hat nicht nur eine Pandemie der Atemwegserkrankungen verursacht, sondern auch die Zahl kardiovaskulärer Komplikationen erheblich gesteigert. Eine differenzierte Diagnostik und Behandlung dieser Komplikationen sind von entscheidender Bedeutung, um die Sterblichkeit zu senken. Die Forschung zu den langfristigen Auswirkungen von COVID-19 auf das Herz-Kreislauf-System muss intensiviert werden, um betroffenen Patienten die bestmögliche Versorgung zu bieten. > Zur Studie

Medical News: SARS-CoV-2 Induces Significant Morphological Changes in the Human Spleen The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has primarily been associated with respiratory complications. However, emerging research indicates that the virus also affects various extrapulmonary organs, including the spleen. Understanding the morphological alterations in the spleen due to SARS-CoV-2 in...

A third of healthcare staff have symptoms consistent with long Covid but only a fraction have a ...

Long COVID is more than just lingering symptoms—it may have a hidden biological basis that standard medical tests fail to detect. A groundbreaking study using advanced MRI technology has uncovered significant lung abnormalities in children and adolescents suffering from long COVID, particularly i

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Environmental surveillance of infectious organisms holds tremendous promise to reduce human-to-human transmission in indoor spaces through early detection. In this study we determined the applicability and limitations of wastewater, indoor high-touch surfaces, in-room air, and rooftop exhaust air sampling methods for detecting SARS-CoV-2 in a real world building occupied by residents recently diagnosed with COVID-19. We concurrently examined the results of three 24-hour environmental surveillance techniques, indoor surface sampling, exhaust air sampling and wastewater surveillance, to the known daily census fluctuations in a COVID-19 isolation dormitory. Additionally, we assessed the ability of aerosol samplers placed in the large volume lobby to detect SARS-CoV-2 multiple times per day. Our research reveals an increase in the number of individuals confirmed positive with COVID-19 as well as their estimated human viral load to be associated with statistically significant increases in viral loads detected in rooftop exhaust aerosol samples (p = 0.0413), wastewater samples (p = 0.0323,), and indoor high-touch surfaces (p < 0.001)). We also report that the viral load detected in lobby aerosol samples was statistically higher in samples collected during presence of occupants whose COVID-19 diagnostic tests were confirmed positive via qPCR compared to periods when the lobby was occupied by either contact-traced (suspected positive) individuals or during unoccupied periods (p = 0.0314 and <2e−16). We conclude that each daily (24h) surveillance method, rooftop exhaust air, indoor high-touch surfaces, and wastewater, provide useful detection signals for building owner/operator(s). Furthermore, we demonstrate that exhaust air sampling can provide spatially resolved signals based upon ventilation exhaust zones. Additionally, we find that indoor lobby air sampling can provide temporally resolved signals useful during short duration sampling periods (e.g., 2-4 hours) even with intermittent occupancy by occupants diagnosed with COVID-19.

Five years on from March 2020, millions of people still face debilitating symptoms, with huge repercussions on public health and productivity. But politicians are starting to pretend the pandemic never happened

Understanding the effects of SARS-CoV-2 infection and COVID-19 vaccination during pregnancy can help inform clinical guidance and tackle vaccine hesitancy. We examined relationships between SARS-CoV-2 infection during pregnancy, COVID-19 vaccination during pregnancy, and early child developmental concerns in children aged 13–15 months in Scotland. Methods We created a large, population-level linked administrative health dataset, combining the COVID-19 in Pregnancy in Scotland (COPS) dataset with age 13–15 month child health review data and other datasets. We included children estimated to have been conceived after May 18, 2020, and born before Sept 30, 2021, and their mothers. We used logistic regression modelling to investigate associations between SARS-CoV-2 infection during pregnancy, COVID-19 vaccination during pregnancy, and developmental concerns (ie, parent or caregiver developmental concerns and health visitor-identified concerns regarding speech–language–communication, problem solving, gross motor, personal–social, and emotional–behavioural development) measured during routine child health reviews at age 13–15 months, including adjustment for confounders and covariates. Findings A total of 24 919 child–mother pairs (12 752 [51·2%] male children; 12 167 [48·8%] female children) were included. 1631 (6·5%) children were prenatally exposed to SARS-CoV-2 and 4943 (19·8%) to COVID-19 vaccination. We found no associations between SARS-CoV-2 infection during pregnancy and developmental concerns. After confounder and covariate adjustment, COVID-19 vaccination during pregnancy was associated with reduced odds of developmental concerns regarding problem solving (odds ratio 0·78 [95% CI 0·64–0·95]), personal–social (0·76 [0·61–0·95]), and emotional–behavioural (0·67 [0·48–0·92]) development, but had no associations with other developmental concerns. Interpretation SARS-CoV-2 infections during pregnancy do not appear to be linked to early childhood developmental concerns, and COVID-19 vaccinations during pregnancy appear to be safe from the perspective of early childhood developmental concerns. As some developmental concerns do not become apparent until children are older than 13–15 months, future research should continue to monitor outcomes as children grow and develop.

Medical News: COVID-19 has been associated with numerous complications, including the deterioration of muscle mass and function, a condition known as sarcopenia. In high-risk patients, the impact of the virus on muscle health can be severe, leading to long-term consequences. A recent clinical study conducted by researchers from Ilam University of Medical Sciences, Tehran University of Medical Scie...

Rund um das Immunsystem gibt es viele Mythen und Missverständnisse. Dieser Text klärt einige häufige Fragen wissenschaftlich fundiert auf.

In this randomized, open-label, positive-controlled trial, eligible participants were allocated to four cohorts: Cohort #1, Cohort #2, Cohort #3, and Cohort #4. Prior to allocation, participants in Cohort #1 and Cohort #2 had received two doses of the inactivated vaccine BBIBP-CorV; those in Cohort #3 had received three doses of the inactivated vaccine BBIBP-CorV; and those in Cohort #4 had received three doses of the recombinant protein vaccine ZF2001. During the trial, participants in Cohort #1 were administered a single dose of the inactivated vaccine BBIBP-CorV, whereas participants in the other cohorts received a single dose of the bivalent recombinant protein vaccine ZF2202. Immunogenicity against Delta, BA.2, and BA.5 subvariants was assessed on day 14 post-vaccination. Results A total of 272 participants were enrolled and allocated to Cohort #1 (N=61), Cohort #2 (N=61), Cohort #3 (N=75), and Cohort #4 (N=75). On day 14 post-vaccination, the geometric mean titers (GMTs) of neutralizing antibodies against the Delta variant increased 14.9-fold, 98.8-fold, 25.8-fold, and 62.8-fold, respectively, across these cohorts. For the BA.2 subvariant, the GMTs increased 6.1, 38.5, 32.7, and 100.1 times, respectively. For the BA.5 subvariant, the GMTs increased 2.7, 14.2, 15.2, and 28.1 times, respectively. Within 28 days after vaccination, the incidences of adverse reactions were 41.7%, 31.2%, 37.3%, and 57.3%, respectively. No serious adverse event and adverse event resulted in withdrawal or death occurred.

This study aimed to explore variations of brain functional connectivity patterns among post-COVID-19 patients with different outcomes of sleep quality. Methods Post-COVID-19 patients were prospectively enrolled and categorized into improvement or deterioration groups based on changes in sleep quality after a three-month follow-up. Functional MRI and blood samples were collected, while a battery of assessments was administered to evaluate sleep quality, mental status, and cognition. Baseline and follow-up data were compared to identify post-infection alterations. Brain functional networks and graph theory analysis were employed to derive network properties, with subsequent investigation into the correlation between these properties, sleep and psychological assessment scores, and blood test outcomes. Results The graph theory analysis revealed a significantly increase in global efficiency (Eglob) and local efficiency (Eloc), and a decrease in λ, in the improvement group. A notable enhancement of frontoparietal network (FPN) were observed. The deterioration group exhibited a significant increase in Eloc and λ, along with a decrease in Eglob. Furthermore, the deterioration group demonstrated a lower level of Eglob at follow-up. With respect to network strength, all networks except FPN showed significantly higher values in the improvement group. Pittsburgh Sleep Quality Index and Self-Rating Anxiety Scale scores differed between two groups. Conclusion Changes in sleep quality following COVID-19 infection are associated with brain functional connectivity patterns. Decreased Eglob is related to worsened sleep quality. The normalized strength of FPN serves as a key indicator for improved sleep quality, while other networks also play roles in regulating sleep quality.

Aims This study aimed to explore the epidemiological circumstances, long-term clinical outcomes, and perceived impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on elite athletes’ sports performance. A secondary objective was to determine the sports-specific (contact vs. noncontact) prevalence of SARS-CoV‑2 among 65 SARS-CoV-2-positive athletes from the Olympic Training Center Rhineland (OSP; n = 599). Methods In all, 65 SARS-CoV-2-positive athletes from the German Olympic Training Center (OSP; 66% males—age: 23 ± 4 years; 34% females—age: 23 ± 5 years) participated in the panel study. Data collection occurred between June 2020 and October 2021 at two test times (t0: after a negative polymerase chain reaction [PCR] test, t1: 16 weeks after t0) through questionnaires and clinical assessments. Results The SARS-CoV‑2 prevalence was nearly identical in noncontact and contact-sport athletes (10.8% vs. 11.3%); 37% experienced symptoms lasting  4 weeks. Over 50% of athletes paused their training for 4–8 weeks. At t1, 40% still experienced reduced perceived performance capacity (PPC) compared to their pre-COVID-19 level, while 64% reported ongoing limitations in sports participation, with mental and physical fatigue as the most prominent limiting factor, followed by shortness of breath and joint and muscle pain. Conclusion The long-term management of SARS-CoV-2-positive elite athletes should involve a comprehensive, multidimensional psychophysiological approach to address persistent sport-restricting symptoms. This approach will assist in developing tailored training protocols that allow a gradual increase in intensity and volume.

This case-control study among US children estimates the association of mRNA COVID-19 vaccination with likelihood of post–COVID-19 condition.

Increased risks of death and hospitalisation for organ disorders after discharge for COVID-19 hospitalisation have been reported but their persistence is unknown. Methods We conducted a nationwide cohort study using the French claims database; subjects hospitalised for COVID-19 between 2020/01/01 and 2020/08/30 were followed up to 30-months and matched to controls from the general population (GP) not hospitalised for COVID-19 during this period. Outcomes were all-cause mortality and organ disorders-related hospitalisation identified using ICD-10 codes. Cumulative incidences were estimated using the Kaplan-Meier method. Incidence rate ratios (IRR) were estimated such as the adjusted sub-distribution hazard ratio on 6-month periods during the follow-up using Cox regressions. Results 63,990 COVID-19 subjects (mean age (SD) 65 years (18), 53.1% male) were matched to 319,891 controls. The weighted cumulative incidences of all-cause mortality and all-cause hospitalisation were 5,218/105 person-years (PY) [95%CI 5,127; 5,305] and 16,334/105 PY [16,162; 16,664] among COVID-19 subjects and 4,013/105 [3,960; 4,047] and 12,095/105 PY [12,024; 12,197] among controls, respectively. COVID-19 subjects were more likely to be hospitalised for cardiovascular (IRR 1.22 [1.15; 1.29]), psychiatric (IRR 1.41 [1.29; 1.53]), neurological (IRR 1.50 [1.41; 1.61]), and respiratory events (IRR 1.99 [1.87; 2.12]). The excess risk strongly decreased after the first 6 months for all outcomes but remained significantly increased up to 30-month for neurological, respiratory disorders, chronic renal failure and diabetes. Conclusions COVID-19 hospitalised subjects were at increased risk of death or hospitalisation for various organ disorders up to 30 months after discharge, reflecting the multi-organ consequences of the disease.

The SARS-CoV-2 pandemic has taught important lessons about the central role of virus-specific CD8+ T cells in mediating antiviral immunity, both during natural infection and following vaccination. In contrast to antibodies, which primarily prevent viral entry, CD8+ T cells exert antiviral functions by recognizing viral peptides presented on infected cells, allowing them to directly kill the virus-infected cells and prevent further viral spread. This is particularly important for individuals with reduced or absent humoral responses. Indeed, virus-specific CD8+ T cell responses induced by infection are associated with improved survival and thus, with a protective role, in immunosuppressed individuals, who have deficient humoral and B cell immunity (1). The protective role of CD8+ T cells during viral infection has further been demonstrated in preclinical models where depletion of CD8+ T cells abrogated viral control and CD8+ T cell transfer improved viral control (2). Moreover, CD8+ T cells have been suggested to play a significant role in the control of emerging viral variants. CD8+ T cells target a broad range of epitopes from both structural and nonstructural proteins of the virus, which are often conserved across different strains (3–5). The breadth of the CD8+ T cell response together with the high level of conservation enables virus-specific CD8+ T cells to cross-recognize various viral variants (4–7), thereby mitigating the impact of mutations that may arise over time. Consequently, a robust CD8+ T cell response can be crucial in maintaining immunity and preventing severe disease, even in the face of viral evolution. Infection- and vaccine-induced CD8+ T cell responses are stable over time and are rapidly reactivated in case of reinfection, hence exhibiting robust memory responses that contribute to long-lasting immunity (8, 9). However, despite these beneficial effects, CD8+ T cells have also been implicated in the pathogenesis of severe COVID-19. They may be involved indirectly by an insufficient ability to limit viral replication and spread or directly through nonspecific effector functions that lead to the killing of uninfected cells and tissue damage. In this minireview, we highlight some of the key features of SARS-CoV-2-specific CD8+ T cell immunity during natural infection and after vaccination that contribute to both viral control and disease pathogenesis.

Localized surface plasmon resonance (LSPR) is an optical phenomenon derived from the dielectric properties of noble metals, resulting in a highly change-sensitive spectrum that can be used on a sensor platform. We have used gold nanorods to develop a diagnostic assay to detect antibodies against the nucleocapsid (N) protein of SARS-CoV-2. This approach is particularly valuable, considering the limited role of serology in recognizing acute infections. Gold nanoparticles were coated with the recombinant N protein and characterized by spectroscopy, fluorometry, and electron microscopy. Positive and negative COVID-19 sera samples were initially categorized through qRT-PCR and further validated using an anti-IgG ELISA. The nanosensor was accurate and able to detect very low levels of anti-SARS-CoV-2 antibodies derived from different virus variants early in infection (before 10 days post-infection). The nanoplatform exhibited high sensitivity and specificity, is suitable for mass production, and has easy implementation and automatic read-out.

COVID19 presented an unprecedented challenge for modern science/medicine. Faced with a novel infectious disease, doctors, scientists, and health officials rose to the challenge in remarkable speed.…

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Among participants followed up to 3 years after initial infection, those with current Long COVID had worse physical and mental health outcomes. The majority of those with Long COVID did not resolve, with less than 2% having resolved Long COVID. The resolved Long COVID cohort had moderately worse physical and mental health compared with those never-having-Long COVID. COVID-19 vaccination was associated with better outcomes.

This cohort study assesses the severity and long-term mortality of COVID-19, influenza, and respiratory syncytial virus in a large cohort of nonhospitalized veterans.