Chikungunya virus (CHIKV) is vectored by Aedes aegypti and Aedes albopictus mosquitoes and is found throughout tropical and sub-tropical regions. While most infections cause mild symptoms such as fever and arthralgia, there have been cases in which cardiac involvement has been reported. In adults, case reports include symptoms ranging from tachycardia and arrythmia, to myocarditis and cardiac arrest. In children, case reports describe symptoms such as arrythmia, myocarditis, and heart failure. Case reports of perinatal and neonatal CHIKV infections have also described cardiovascular compromise, including myocardial hypertrophy, ventricular dysfunction, myocarditis, and death. Myocarditis refers to inflammation of the heart tissue, which can be caused by viral infection, thus becoming viral myocarditis. Since viral myocarditis is linked as a causative factor of other cardiomyopathies, including dilated cardiomyopathy, in which the heart muscle weakens and fails to pump blood properly, the connection between CHIKV and the heart is concerning. We searched Pubmed, Embase, LILACS, and Google Scholar to identify case reports of CHIKV infections where cardiac symptoms were reported. We utilized NCBI Virus and NCBI Nucleotide to explore the lineage/evolution of strains associated with these outbreaks. Statistical analysis was performed to identify which clinical features were associated with death. Phylogenetic analysis determined that CHIKV infections with cardiac symptoms are associated with the Asian, the East Central South African, and the Indian Ocean lineages. Of patients admitted to hospital, death rates ranged from 26–48%. Myocarditis, hypertension, pre-existing conditions, and the development of heart failure were significantly correlated with death. As such, clinicians should be aware in their treatment and follow-up of patients.
(1) Background: The human brain is of interest in viral research because it is often the target of viruses. Neurological infections can result in consequences in the CNS, which can result in death or lifelong sequelae. Organoids modeling the CNS are notable because they are derived from stem cells that differentiate into specific brain cells such as neural progenitors, neurons, astrocytes, and glial cells. Numerous protocols have been developed for the generation of CNS organoids, and our goal was to describe the various CNS organoid models available for viral pathogenesis research to serve as a guide to determine which protocol might be appropriate based on research goal, timeframe, and budget. (2) Methods: Articles for this review were found in Pubmed, Scopus and EMBASE. The search terms used were “brain + organoid” and “CNS + organoid” (3) Results: There are two main methods for organoid generation, and the length of time for organoid generation varied from 28 days to over 2 months. The costs for generating a population of organoids ranged from USD 1000 to 5000. (4) Conclusions: There are numerous methods for generating organoids representing multiple regions of the brain, with several types of modifications for fine-tuning the model to a researcher’s specifications. Organoid models of the CNS can serve as a platform for characterization and mechanistic studies that can reduce or eliminate the use of animals, especially for viruses that only cause disease in the human CNS.
Dengue virus (DENV) is a flavivirus that is a significant cause of human disease costing billions of dollars per year in medical and mosquito control costs. It is estimated that up to 20% of DENV infections affect the brain. Incidence of DENV infections is increasing, which suggests more people are at risk of developing neurological complications. The most common neurological manifestations of DENV are encephalitis and encephalopathy, and movement disorders such as parkinsonism have been observed. Parkinsonism describes syndromes similar to Parkinson’s Disease where tremors, stiffness, and slow movements are observed. Parkinsonism caused by viral infection is characterized by patients exhibiting at least two of the following symptoms: tremor, bradykinesia, rigidity, and postural instability. To investigate DENV-associated parkinsonism, case studies and reports of DENV-associated parkinsonism were obtained from peer-reviewed manuscripts and gray literature. Seven reports of clinically diagnosed DENV-associated parkinsonism and 15 cases of DENV encephalitis, where the patient met the case criteria for a diagnosis of viral parkinsonism were found. Clinically diagnosed DENV-associated parkinsonism patients were more likely to be male and exhibit expressionless face, speech problems, and lymphocytosis. Suspected patients were more likely to exhibit tremor, have thrombocytopenia and low hemoglobin. Viral parkinsonism can cause a permanent reduction in neurons with consequential cognitive and behavior changes, or it can leave a latent imprint in the brain that can cause neurological dysfunction decades after recovery. DENV-associated parkinsonism is underdiagnosed and better adherence to the case definition of viral parkinsonism is needed for proper management of potential sequalae especially if the patient has an ongoing or potential to develop a neurodegenerative disease.
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