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JC polyomavirus (JCPyV) is a human-specific polyomavirus that establishes a silent lifelong infection in multiple peripheral organs, predominantly those of the urinary tract, of immunocompetent individuals. In immunocompromised settings, however, JCPyV can infiltrate the central nervous system (CNS), where it causes several encephalopathies of high morbidity and mortality. JCPyV-induced progressive multifocal leukoencephalopathy (PML), a devastating demyelinating brain disease, was an AIDS-defining illness before antiretroviral therapy that has “reemerged” as a complication of immunomodulating and chemotherapeutic agents. No effective anti-polyomavirus therapeutics are currently available. How depressed immune status sets the stage for JCPyV resurgence in the urinary tract, how the virus evades pre-existing antiviral antibodies to become viremic, and where/how it enters the CNS are incompletely understood. Addressing these questions requires a tractable animal model of JCPyV CNS infection. Although no animal model can replicate all aspects of any human disease, mouse polyomavirus (MuPyV) in mice and JCPyV in humans share key features of peripheral and CNS infection and antiviral immunity. In this review, we discuss the evidence suggesting how JCPyV migrates from the periphery to the CNS, innate and adaptive immune responses to polyomavirus infection, and how the MuPyV-mouse model provides insights into the pathogenesis of JCPyV CNS disease. Full article

The JC polyomavirus virus (JCPyV) affects more than 80% of the human population in their early life stage. It mainly affects immunocompromised individuals where virus replication in oligodendrocytes and astrocytes may lead to fatal progressive multifocal encephalopathy (PML). Virus protein 1 (VP1) is one of the major structural proteins of the viral capsid, responsible for keeping the virus alive in the gastrointestinal and urinary tracts. VP1 is often targeted for antiviral drug and vaccine development. Similarly, this study implied immune-informatics and molecular modeling methods to design a multi-epitope subunit vaccine targeting JCPyV. The VP1 protein epitopic sequences, which are highly conserved, were used to build the vaccine. This designed vaccine includes two adjuvants, five HTL epitopes, five CTL epitopes, and two BCL epitopes to stimulate cellular, humoral, and innate immune responses against the JCPyV. Furthermore, molecular dynamics simulation (100 ns) studies were used to examine the interaction and stability of the vaccine protein with TLR4. Trajectory analysis showed that the vaccine and TLR4 receptor form a stable complex. Overall, this study may contribute to the path of vaccine development against JCPyV. Full article

Background and Objectives: Central nervous system (CNS) disorders are estimated to occur in approximately 10–20% of people living with HIV (PLWH). They are more commonly observed in newly diagnosed patients and in previously untreated patients or those refusing to undergo antiretroviral treatment. CNS diseases can also be the first manifestation of HIV/AIDS infection. The most common HIV-related central nervous system diseases (CNS-D) are CNS toxoplasmosis, CNS cryptococcosis, progressive multifocal leukoencephalopathy (PML), and HIV-associated encephalopathy treated as a neurocognitive disorder. Materials and Methods: A retrospective analysis of available medical records was performed on 476 patients hospitalised over a period from 2016 to 2021 and diagnosed with HIV/AIDS infection at the department of infectious diseases at the Provincial Specialist Hospital in Wroclaw. An additional criterion for selecting patients for the analysis was the performance of head imaging using computed tomography or magnetic resonance imaging on prospective patients. Results: Neurotoxoplasmosis, neurocryptococcosis, progressive multifocal leukoencephalopathy (PML), and neurosyphilis were the most common CNS diseases among the analysed group of patients. Based on radiological descriptions, other abnormalities, such as vascular changes or cortical and subcortical atrophy of multifactorial origin, not exclusively related to HIV infection, were also frequently observed. The most common neurological symptoms reported in the study group were headaches, limb paresis, and gait and balance disturbance. Conclusions: The clinical picture and epidemiology of neurological manifestations in the group of HIV-infected patients under assessment were similar to the results of other authors. Given the current epidemiological situation, diagnosis for HIV infection should be considered in patients admitted to neurological departments. Full article