1.
Ross River Virus Immune Evasion Strategies and the Relevance to Post-viral Fatigue, and Myalgic Encephalomyelitis Onset.
Lidbury, BA
Frontiers in medicine. 2021;8:662513
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Plain language summary
Ross river virus (RRV) is a mosquito borne virus that is thought to be the trigger of myalgic encephalomyelitis (ME) in many Australians. Viruses like RRV are thought to be so successful due to their ability to avoid and often manipulate the hosts immune response. This review of 75 studies aimed to discuss immune evasion strategies employed by RRV and understand the relevance to post viral fatigue and the development of ME. The authors began by explaining how RRV manipulates the hosts immune system to gain entry to cells and replicate. Once the virus has entered the cells, it is thought that it disrupts inflammatory pathways and decreases anti-viral genes. Disruption of inflammation has also been reported to affect energy production in individuals with ME. It was concluded that viruses such as RRV can manipulate the hosts immune system resulting in disruption of energy production. Understanding these pathways and interactions may explain why some individuals go on to develop ME post infection and others do not. Findings may also help to understand ME like symptoms reported by some patients who have recovered from Covid-19. This paper could be used by healthcare professionals to understand the development of ME and fatigue symptoms in individuals who have recovered from viruses such as RRV and Covid-19.
Abstract
Ross River virus (RRV) is an endemic Australian arbovirus, and member of the Alphavirus family that also includes Chikungunya virus (CHIK). RRV is responsible for the highest prevalence of human disease cases associated with mosquito-borne transmission in Australia, and has long been a leading suspect in cases of post-viral fatigue syndromes, with extrapolation of this link to Myalgic Encephalomyelitis (ME). Research into RRV pathogenesis has revealed a number of immune evasion strategies, impressive for a virus with a genome size of 12 kb (plus strand RNA), which resonate with insights into viral pathogenesis broadly. Drawing from observations on RRV immune evasion, mechanisms of relevance to long term idiopathic fatigue are featured as a perspective on infection and eventual ME symptoms, which include considerations of; (1) selective pro-inflammatory gene suppression post antibody-dependent enhancement (ADE) of RRV infection, (2) Evidence from other virus families of immune disruption and evasion post-ADE, and (3) how virally-driven immune evasion may impact on mitochondrial function via target of rapamycin (TOR) complexes. In light of these RRV measures to counter the host immune - inflammatory responses, links to recent discoveries explaining cellular, immune and metabolomic markers of ME will be explored and discussed, with the implications for long-COVID post SARS-CoV-2 also considered. Compelling issues on the connections between virally-induced alterations in cytokine expression, for example, will be of particular interest in light of energy pathways, and how these perturbations manifest clinically.
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Prevalence, Severity and Mortality associated with COPD and Smoking in patients with COVID-19: A Rapid Systematic Review and Meta-Analysis.
Alqahtani, JS, Oyelade, T, Aldhahir, AM, Alghamdi, SM, Almehmadi, M, Alqahtani, AS, Quaderi, S, Mandal, S, Hurst, JR
PloS one. 2020;15(5):e0233147
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This meta-analysis reviewed 15 studies covering a total of 2473 confirmed COVID-19 patients to summarise the potential risk factors for smokers and patients with chronic obstructive pulmonary disease (COPD), a dysfunction of the lung associated with limitation in airflow. They found that neither COPD or smoking increased the initial risk of contracting COVID-19 with only 2% and 9% respectively of the cases falling into these categories. However, both groups had increased risk of developing more servere forms of COVID-19 requiring hospitalisation, admission to Intensive Care Units (ICU), mechanical ventilation, and ultimately death, with a much higher mortality rate of 60% versus other patients. Current smokers were also shown to have double the risk of complications versus ex-smokers. The most severe cases were generally in the older age brackets, with coexisting comorbidities and a hypothesized greater amount of lung damage. Both groups showed signs of acute inflammation and had a much slower recovery compared to non-smokers and patients without COPD. Despite the low prevalence of these groups contracting COVID-19, these people should be considered vulnerable because of the severity of symptoms and greater burden on healthcare.
Abstract
BACKGROUND Coronavirus disease 2019 (COVID-19) is an evolving infectious disease that dramatically spread all over the world in the early part of 2020. No studies have yet summarized the potential severity and mortality risks caused by COVID-19 in patients with chronic obstructive pulmonary disease (COPD), and we update information in smokers. METHODS We systematically searched electronic databases from inception to March 24, 2020. Data were extracted by two independent authors in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Study quality was assessed using a modified version of the Newcastle-Ottawa Scale. We synthesized a narrative from eligible studies and conducted a meta-analysis using a random-effects model to calculate pooled prevalence rates and 95% confidence intervals (95%CI). RESULTS In total, 123 abstracts were screened and 61 full-text manuscripts were reviewed. A total of 15 studies met the inclusion criteria, which included a total of 2473 confirmed COVID-19 patients. All studies were included in the meta-analysis. The crude case fatality rate of COVID-19 was 7.4%. The pooled prevalence rates of COPD patients and smokers in COVID-19 cases were 2% (95% CI, 1%-3%) and 9% (95% CI, 4%-14%) respectively. COPD patients were at a higher risk of more severe disease (risk of severity = 63%, (22/35) compared to patients without COPD 33.4% (409/1224) [calculated RR, 1.88 (95% CI, 1.4-2.4)]. This was associated with higher mortality (60%). Our results showed that 22% (31/139) of current smokers and 46% (13/28) of ex-smokers had severe complications. The calculated RR showed that current smokers were 1.45 times more likely [95% CI: 1.03-2.04] to have severe complications compared to former and never smokers. Current smokers also had a higher mortality rate of 38.5%. CONCLUSION Although COPD prevalence in COVID-19 cases was low in current reports, COVID-19 infection was associated with substantial severity and mortality rates in COPD. Compared to former and never smokers, current smokers were at greater risk of severe complications and higher mortality rate. Effective preventive measures are required to reduce COVID-19 risk in COPD patients and current smokers.