It is well known the potential of severe acute respiratory coronavirus type 2 (SARS-CoV-2) infection to induce post-acute sequelae, a condition called Long COVID. This syndrome includes several symptoms, but the central nervous system (CNS) main one is neurocognitive dysfunction. Recently it has been demonstrated the relevance of plasma levels of neurofilament light chain (pNfL), as a biomarker of early involvement of the CNS in COVID-19. The aim of this study was to investigate the relationship between pNfL in patients with post-acute neurocognitive symptoms and the potential of NfL as a prognostic biomarker in these cases. A group of 63 long COVID patients ranging from 18 to 59 years-old were evaluated, submitted to a neurocognitive battery assessment, and subdivided in different groups, according to results. Plasma samples were collected during the long COVID assessment and used for measurement of pNfL with the Single molecule array (SIMOA) assays. Levels of pNfL were significantly higher in long COVID patients with neurocognitive symptoms when compared to HC (p = 0.0031). Long COVID patients with cognitive impairment and fatigue symptoms presented higher pNfL levels when compared to long COVID patients without these symptoms, individually and combined (p = 0.0263, p = 0.0480, and 0.0142, respectively). Correlation analysis showed that levels of cognitive lost and exacerbation of fatigue in the neurocognitive evaluation had a significative correlation with higher pNfL levels (p = 0.0219 and 0.0255, respectively). Previous reports suggested that pNfL levels are related with higher risk of severity and predict lethality of COVID-19. Our findings demonstrate that SARS-CoV-2 infection seems to have a long-term impact on the brain, even in patients who presented mild acute disease. NfL measurements might be useful to identify CNS involvement in long COVID associated with neurocognitive symptoms and to identify who will need continuous monitoring and treatment support.

SARS-CoV-2 can trigger autoimmune central nervous system (CNS) diseases in genetically susceptible individuals, a mechanism poorly understood. Molecular mimicry (MM) has been identified in other viral diseases as potential triggers of autoimmune CNS events. This study investigated if MM is the process through which SARS-CoV-2 induces the breakdown of immune tolerance. The frequency of autoimmune CNS disorders was evaluated in a prospective cohort with patients admitted to the COVID-19 Intense Care Unity (ICU) in Rio de Janeiro. Then, an in silico analysis was performed to identify the conserved regions that share a high identity between SARS-CoV-2 antigens and human proteins. The sequences with significant identity and antigenic properties were then assessed for their binding capacity to HLA subtypes. Of the 112 patients included, 3 were classified as having an autoimmune disorder. A total of eleven combinations had significant linear and three-dimensional overlap. NMDAR1, MOG, and MPO were the self-antigens with more significant combinations, followed by GAD65. All sequences presented at least one epitope with strong or intermediate binding capacity to the HLA subtypes selected. This study underscores the possibility that CNS autoimmune attacks observed in COVID-19 patients, including those in our population, could be driven by MM in genetically predisposed individuals.

To assess the prevalence of hepatitis E virus (HEV) RNA and antibodies among kidney transplant recipients (KTR) in Central Brazil. The presence of chronic HEV infection was also investigated. A cohort study was conducted among 316 KTR treated at a referral center for kidney transplantation in Goiânia, Brazil. All serum samples were tested for the presence of HEV RNA (real-time PCR) and anti-HEV IgG/IgM (ELISA). Anti-HEV-positive samples were confirmed using an immunoblot test. HEV chronicity was investigated in a subgroup of patients with elevated alanine aminotransferase (ALT >40IU/l) through HEV RNA detection in additional serum samples collected 3 and 6 months apart. A seroprevalence of 2.5% (95% confidence interval 1.2-5.1%) was found for anti-HEV IgG. There was no difference in characteristics between the anti-HEV IgG seropositive and seronegative KTR groups. Anti-HEV IgM was detected in only one patient (0.3%). All KTR were negative for HEV RNA. These results show that HEV infection is infrequent in KTR in Central Brazil, with low seroprevalence rates of past and recent infection, and also an absence of active and chronic HEV infections.

Aims To improve RT‐qPCR with an internal control and a synthetic standard curve to detect HEV in HIV co‐infected patients. Methods and Results A single‐stranded RNA (ssRNA) and a double‐stranded DNA (dsDNA) synthetic curve were designed, compared to the international reference panel for HEV genotypes, and tested to quantify and detect a reference panel for HEV genotypes. The detection limit of the RNA synthetic curve (50 copies per ml) was better than the DNA synthetic curve (100 copies per ml) and the WHO standard curve (250 copies per ml). Then, 280 serum samples from HIV‐positive patients were tested for HEV RNA, which was detected in 3·6% of serum samples. The viral load ranged from 2 × 10² copies per ml to 4·78 × 10⁸ copies per ml. HEV IgM/IgG antibodies were not detected in the RNA‐positive patients. Sequencing analysis of HEV showed that the virus belongs to genotype 3 (HEV GT3). Conclusions Real‐time PCR was a useful tool to estimate co‐infection with HEV/HIV, even in patients with low viral loads and undetectable anti‐HEV IgG and IgM antibodies. Significance and Impact of the Study Hepatitis E virus genotype 3 (HEV GT3) has been associated with silent chronic hepatitis and cirrhosis in HIV‐positive subjects worldwide, but there is a lack of data on this co‐infection in Brazil.

Since COVID-19 was declared a pandemic, Brazil has become one of the countries most affected by this disease. A year into the pandemic, a second wave of COVID-19 emerged, with a rapid spread of a new SARS-CoV-2 lineage of concern. Several vaccines have been granted emergency-use authorization, leading to a decrease in mortality and severe cases in many countries. However, the emergence of SARS-CoV-2 variants raises the alert for potential new waves of transmission and an increase in pathogenicity. We compared the demographic and clinical data of critically ill patients infected with COVID-19 hospitalized in Rio de Janeiro during the first and second waves between July 2020 and October 2021. In total, 106 participants were included in this study; among them, 88% had at least one comorbidity, and 37% developed severe disease. Disease severity was associated with older age, pre-existing neurological comorbidities, higher viral load, and dyspnea. Laboratory biomarkers related to white blood cells, coagulation, cellular injury, inflammation, renal, and liver injuries were significantly associated with severe COVID-19. During the second wave of the pandemic, the necessity of invasive respiratory support was higher, and more individuals with COVID-19 developed acute hepatitis, suggesting that the progression of the second wave resulted in an increase in severe cases. These results can contribute to understanding the behavior of the COVID-19 pandemic in Brazil and may be helpful in predicting disease severity, which is a pivotal for guiding clinical care, improving patient outcomes, and defining public policies.