Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). Compared to other types of self-limiting myelin disorders, MS compartmentalizes and maintains chronic inflammation in the CNS. Even though the exact cause of MS is unclear, it is assumed that genetic and environmental factors play an important role in susceptibility to this disease. The progression of MS is triggered by certain environmental factors, such as viral infections. The most important viruses that affect MS are Epstein-Barr virus (EBV), human herpes virus 6 (HHV-6), human endogenous retrovirus (HERV), cytomegalovirus (CMV), and varicella zoster virus (VZV). These viruses all have latent stages that allow them to escape immune detection and reactivate after exposure to various stimuli. Furthermore, their tropism for CNS and immune system cells explains their possible deleterious function in neuroinflammation. In this study, the effect of viral infections on MS disease focuses on the details of viruses that can change the risk of the disease. Paying attention to the most recent articles on the role of SARS-CoV-2 in MS disease, laboratory indicators show the interaction of the immune system with the virus. Also, strategies to prevent viruses that play a role in triggering MS are discussed, such as EBV, which is one of the most important. 

/pdf/comprehensive-investigations-relationship-between-viral-312cdy2s.pdf

Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis

Accumulating evidence shows that SARS‐CoV‐2 can potentially trigger autoimmune processes, which can be responsible for the long‐term consequences of COVID‐19. Therefore, this paper aims to review the autoantibodies reported in COVID‐19 convalescents. Six main groups were distinguished: (i) autoantibodies against components of the immune system, (ii) autoantibodies against components of the cardiovascular system, (iii) thyroid autoantibodies, (iv) autoantibodies specific for rheumatoid diseases, (v) antibodies against G‐protein coupled receptors, and (vi) other autoantibodies. The evidence reviewed here clearly highlights that SARS‐CoV‐2 infection may induce humoral autoimmune responses. However, the available studies share number of limitations, such as: (1) the sole presence of autoantibodies does not necessarily implicate the clinically‐relevant risks, (2) functional investigations were rarely performed and it is often unknown whether observed autoantibodies are pathogenic, (3) the control seroprevalence, in healthy, noninfected individuals was often not reported; thus it is sometimes unknown whether the detected autoantibodies are the result of SARS‐CoV‐2 infection or the accidental post‐COVID‐19 detection, (4) the presence of autoantibodies was rarely correlated with symptoms of the post‐COVID‐19 syndrome, (5) the size of the studied groups were often small, (6) the studies focused predominantly on adult populations, (7) age‐ and sex‐related differences in seroprevalence of autoantibodies were rarely explored, (8) genetic predispositions that may be involved in generation of autoantibodies during SARS‐CoV‐2 infections were not investigated, and (9) the autoimmune reactions following infection with SARS‐CoV‐2 variants that vary in the clinical course of infection remain unexplored. Further longitudinal studies are advocated to assess the link between identified autoantibodies and particular clinical outcomes in COVID‐19 convalescents.

Overview of autoantibodies in COVID‐19 convalescents

http://www.cell.com/article/S258900422301012X/pdf

Biological mechanisms underpinning the development of long COVID

The aim of this study was to compare the effectiveness of traditional neurological rehabilitation and neurological rehabilitation combined with a rehabilitation robot for patients with post-COVID-19 fatigue syndrome. Eighty-six participants transferred from intensive care units due to post-viral fatigue after COVID-19 were randomly divided into two groups: the intervention group and the control group. The control group received standard neurological rehabilitation for 120 min a day, while the intervention group received the same neurological rehabilitation for 75 min a day, complemented by 45 min of exercises on the rehabilitation robot. The Berg scale, Tinetti scale, six-minute walking test, isokinetic muscle force test, hand grip strength, Barthel Index, and Functional Independence Measure were used to measure the outcomes. Both groups improved similarly during the rehabilitation. Between groups, a comparison of before/after changes revealed that the intervention group improved better in terms of Functional Independence Measure (p = 0.015) and mean extensor strength (p = 0.023). The use of EMG-driven robots in the rehabilitation of post-COVID-19 fatigue syndrome patients was shown to be effective.

The Effect of Using a Rehabilitation Robot for Patients with Post-Coronavirus Disease (COVID-19) Fatigue Syndrome

Rise of life-threatening superbugs, pandemics and epidemics warrants the need for cost-effective and novel pharmacological interventions. Availability of publicly available proteomes of pathogens supports development of high-throughput discovery platforms to prioritize potential drug-targets and develop testable hypothesis for pharmacological screening. The pipeline builder for identification of target (PBIT) was developed in 2016 and updated in 2021, with the purpose of accelerating the search for drug-targets by integration of methods like comparative and subtractive genomics, essentiality/virulence and druggability analysis. Since then, it has been used for identification of drugs and vaccine targets, safety profiling of multiepitope vaccines and mRNA vaccine construction against a broad-spectrum of pathogens. This tool has now been updated with functionalities related to systems biology and immuno-informatics and validated by analysing 48 putative antigens of Mycobacterium tuberculosis documented in literature. PBITv3 available as both online and offline tools will enhance drug discovery against emerging drug-resistant infectious agents. PBITv3 can be freely accessed at http://pbit3.bicnirrh.res.in/offline.php. This article is protected by copyright. All rights reserved.

PBITV3 : A robust and comprehensive tool for screening pathogenic proteomes for drug targets and prioritizing vaccine candidates.

Coronavirus Disease 2019 (COVID-19), caused by the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), persists as a threat to global health and continues to be a rapidly evolving condition. Although COVID19 is negatively correlated with the existing comorbidities in terms of the clinical outcome, the ability of SARS-CoV-2 to mediate the novel, or to exacerbate the existing autoimmune conditions, has generated considerable interest, due to its potential implications both with regard to patients suffering from autoimmune conditions, as well as to the long-term consequences of the disease. However, although molecular mimicry has been postulated as a potential causative factor in post-COVID19 autoimmunity and multi-organ damage, a substantial body of research needs to emerge in order to achieve a more definitive conclusion. We investigated the possibility of SARS-CoV-2 peptide sequences behaving as molecular mimics with a potential to trigger an autoimmune response. Thus, on the basis of analysis in silico, we were able to develop a plausible case for the molecular mimicry as a potential aetiological mechanism of SARS-CoV-2-mediated autoimmunity, both in a multi-organ damage context or outside of the viral phase of infection. Interestingly, this is the first time that the peptide sequence of MACROD1 has been implicated in the COVID-19 autoimmunity. Additionally, we also confirm that PARP9 and PARP14 may be involved in the process.

/pdf/the-possible-role-of-molecular-mimicry-in-sars-cov-2-4rpytlo1ze.pdf

The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis

Human monkeypox represents a relatively underexplored infection that has received increased attention since the reported outbreak in May 2022. Due to its clinical similarities with human smallpox, this virus represents a potentially tremendous health problem demanding further research in the context of host-pathogen interactions and vaccine development. Furthermore, the cross-continental spread of monkeypox has reaffirmed the need for devoting attention to human poxviruses in general, as they represent potential bioterrorism agents. Currently, smallpox vaccines are utilized in immunization efforts against monkeypox, an unsurprising fact considering their genomic and phenotypic similarities. Though it offers long-lasting protection against smallpox, its protective effects against human monkeypox continue to be explored, with encouraging results. Taking this into account, this works aims at utilizing in silico tools to identify potent peptide-based epitopes stemming from the variola virus and monkeypox virus proteomes, to devise a vaccine that would offer significant protection against smallpox and monkeypox. In theory, a vaccine that offers cross-protection against variola and monkeypox would also protect against related viruses, at least in severe clinical manifestation. Herein, we introduce a novel multi-epitope mRNA vaccine design that exploits these two viral proteomes to elicit long-lasting humoral and cellular immunity. Special consideration was taken in ensuring that the vaccine candidate elicits a Th1 immune response, correlated with protection against clinically severe disease for both viruses. Immune system simulations and physicochemical and safety analyses characterize our vaccine candidate as antigenically potent, safe, and overall stable. The protein product displays high binding affinity towards relevant immune receptors. Furthermore, the vaccine candidate is to elicit a protective, humoral and Th1-dominated cellular immune response that lasts over five years. Lastly, we build a case about the rapidity and convenience of circumventing the live attenuated vaccine platform using mRNA vaccine technology.

Multi-epitope mRNA Vaccine Design that Exploits Variola Virus and Monkeypox Virus Proteins for Elicitation of Long-lasting Humoral and Cellular Protection Against Severe Disease

Modeling of food transport and absorption inside the small intestine is essential to better understand the digestive process as a whole. The models described by our paper present a method to visualize transport of a mass of food representing a bolus from the pylorus to the edge of the ileum. We have developed an integrated model to demonstrate passage of the bolus through the small intestine as well as the absorption of nutrients from it. We also aim to briefly discuss the importance of intestinal modeling, the models that have been developed including those we have based our own models on, and limitations of intestinal modeling as opposed to in vivo studies. Finally, we discuss future directions that intestinal modeling researchers can explore, such as inclusion of other organs within the digestive system and more specific modeling applying to different types of foods.

Simulating Passage and Absorption of Bolus with an Emphasis on the Small Intestine Using a MultiComponent Model

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The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis

Multi-epitope mRNA Vaccine Design that Exploits Variola Virus and Monkeypox Virus Proteins for Elicitation of Long-lasting Humoral and Cellular Protection Against Severe Disease

Simulating Passage and Absorption of Bolus with an Emphasis on the Small Intestine Using a MultiComponent Model