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1.
Rev Esp Quimioter ; 34 Suppl 1: 69-71, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1449589

ABSTRACT

There are few publications on the impact of coinfection and superinfection in patients with COVID-19. Patients with higher severity are much more prone to secondary bacterial, fungal or viral infections. The overuse of antimicrobials in many viral infections (including SARS-CoV-2 infections) undoubtedly contributes to the current antimicrobial resistance crisis. In the context of COVID-19, we are witnessing an increase in multidrug-resistant bacterial infections in our hospitals. The heterogeneity of published studies makes it critical to perform more large-scale studies to better understand the pathogenesis of coinfections or superinfections in the COVID-19 patient.


Subject(s)
COVID-19 , Coinfection , Superinfection , Virus Diseases , Humans , SARS-CoV-2 , Virus Diseases/complications
2.
Front Immunol ; 12: 722979, 2021.
Article in English | MEDLINE | ID: covidwho-1399139

ABSTRACT

The immunopathology of type I diabetes (T1D) presents a complicated case in part because of the multifactorial origin of this disease. Typically, T1D is thought to occur as a result of autoimmunity toward islets of Langerhans, resulting in the destruction of insulin-producing cells (ß cells) and thus lifelong reliance on exogenous insulin. However, that explanation obscures much of the underlying mechanism, and the actual precipitating events along with the associated actors (latent viral infection, diverse immune cell types and their roles) are not completely understood. Notably, there is a malfunctioning in the regulation of cytotoxic CD8+ T cells that target endocrine cells through antigen-mediated attack. Further examination has revealed the likelihood of an imbalance in distinct subpopulations of tolerogenic and cytotoxic natural killer (NK) cells that may be the catalyst of adaptive immune system malfunction. The contributions of components outside the immune system, including environmental factors such as chronic viral infection also need more consideration, and much of the recent literature investigating the origins of this disease have focused on these factors. In this review, the details of the immunopathology of T1D regarding NK cell disfunction is discussed, along with how those mechanisms stand within the context of general autoimmune disorders. Finally, the rarer cases of latent autoimmune, COVID-19 (viral), and immune checkpoint inhibitor (ICI) induced diabetes are discussed as their exceptional pathology offers insight into the evolution of the disease as a whole.


Subject(s)
Autoimmune Diseases/immunology , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/pathology , Killer Cells, Natural/immunology , Killer Cells, Natural/pathology , Autoantibodies/immunology , Autoimmune Diseases/pathology , COVID-19/complications , Diabetes Mellitus, Type 1/etiology , Humans , Insulin/metabolism , Insulin-Secreting Cells/immunology , Virus Diseases/complications
3.
Front Immunol ; 12: 659419, 2021.
Article in English | MEDLINE | ID: covidwho-1389180

ABSTRACT

Highly pathogenic virus infections usually trigger cytokine storms, which may have adverse effects on vital organs and result in high mortalities. The two cytokines interleukin (IL)-4 and interferon (IFN)-γ play key roles in the generation and regulation of cytokine storms. However, it is still unclear whether the cytokine with the largest induction amplitude is the same under different virus infections. It is unknown which is the most critical and whether there are any mathematical formulas that can fit the changing rules of cytokines. Three coronaviruses (SARS-CoV, MERS-CoV, and SARS-CoV-2), three influenza viruses (2009H1N1, H5N1 and H7N9), Ebola virus, human immunodeficiency virus, dengue virus, Zika virus, West Nile virus, hepatitis B virus, hepatitis C virus, and enterovirus 71 were included in this analysis. We retrieved the cytokine fold change (FC), viral load, and clearance rate data from these highly pathogenic virus infections in humans and analyzed the correlations among them. Our analysis showed that interferon-inducible protein (IP)-10, IL-6, IL-8 and IL-17 are the most common cytokines with the largest induction amplitudes. Equations were obtained: the maximum induced cytokine (max) FC = IFN-γ FC × (IFN-γ FC/IL-4 FC) (if IFN-γ FC/IL-4 FC > 1); max FC = IL-4 FC (if IFN-γ FC/IL-4 FC < 1). For IFN-γ-inducible infections, 1.30 × log2 (IFN-γ FC) = log10 (viral load) - 2.48 - 2.83 × (clearance rate). The clinical relevance of cytokines and their antagonists is also discussed.


Subject(s)
Cytokine Release Syndrome/immunology , Cytokines/blood , Models, Immunological , Virus Diseases/complications , Biomarkers/blood , Biomarkers/metabolism , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/diagnosis , Cytokine Release Syndrome/virology , Cytokines/immunology , Cytokines/metabolism , Humans , Viral Load/immunology , Virus Diseases/blood , Virus Diseases/immunology , Virus Diseases/virology
4.
Sci Rep ; 11(1): 8968, 2021 04 26.
Article in English | MEDLINE | ID: covidwho-1387471

ABSTRACT

A significant number of studies invoked diabetes as a risk factor for virus infections, but the issue remains controversial. We aimed to examine whether non-autoimmune diabetes mellitus enhances the risk of virus infections compared with the risk in healthy individuals without non-autoimmune diabetes mellitus. In this systematic review and meta-analysis, we assessed case-control and cohort studies on the association between non-autoimmune diabetes and viruses. We searched PubMed, Embase, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, and Web of Science with no language restriction, to identify articles published until February 15, 2021. The main outcome assessment was the risk of virus infection in individuals with non-autoimmune diabetes. We used a random-effects model to pool individual studies and assessed heterogeneity (I2) using the χ2 test on Cochrane's Q statistic. This study is registered with PROSPERO, number CRD42019134142. Out of 3136 articles identified, we included 68 articles (90 studies, as the number of virus and or diabetes phenotype varied between included articles). The summary OR between non-autoimmune diabetes and virus infections risk were, 10.8(95% CI: 10.3-11.4; 1-study) for SARS-CoV-2; 3.6(95%CI: 2.7-4.9, I2 = 91.7%; 43-studies) for HCV; 2.7(95% CI: 1.3-5.4, I2 = 89.9%, 8-studies;) for HHV8; 2.1(95% CI: 1.7-2.5; 1-study) for H1N1 virus; 1.6(95% CI: 1.2-2.13, I2 = 98.3%, 27-studies) for HBV; 1.5(95% CI: 1.1-2.0; 1-study) for HSV1; 3.5(95% CI: 0.6-18.3 , I2 = 83.9%, 5-studies) for CMV; 2.9(95% CI: 1-8.7, 1-study) for TTV; 2.6(95% CI: 0.7-9.1, 1-study) for Parvovirus B19; 0.7(95% CI: 0.3-1.5 , 1-study) for coxsackie B virus; and 0.2(95% CI: 0-6.2; 1-study) for HGV. Our findings suggest that, non-autoimmune diabetes is associated with increased susceptibility to viruses especially SARS-CoV-2, HCV, HHV8, H1N1 virus, HBV and HSV1. Thus, these viruses deserve more attention from diabetes health-care providers, researchers, policy makers, and stakeholders for improved detection, overall proper management, and efficient control of viruses in people with non-autoimmune diabetes.


Subject(s)
Diabetes Complications , Virus Diseases/complications , Case-Control Studies , Cohort Studies , Humans , Risk Factors
6.
Biochim Biophys Acta Rev Cancer ; 1876(2): 188622, 2021 12.
Article in English | MEDLINE | ID: covidwho-1377662

ABSTRACT

Since the identification of the first human oncogenic virus in 1964, viruses have been studied for their potential role in aiding the development of cancer. Through the modulation of cellular pathways associated with proliferation, immortalization, and inflammation, viral proteins can mimic the effect of driver mutations and contribute to transformation. Aside from the modulation of signaling pathways, the insertion of viral DNA into the host genome and the deregulation of cellular miRNAs represent two additional mechanisms implicated in viral oncogenesis. In this review, we will discuss the role of twelve different viruses on cancer development and how these viruses utilize the abovementioned mechanisms to influence oncogenesis. The identification of specific mechanisms behind viral transformation of human cells could further elucidate the process behind cancer development.


Subject(s)
Cell Transformation, Neoplastic/genetics , Neoplasms/etiology , Neoplasms/virology , Virus Diseases/complications , Humans , Virus Diseases/pathology
7.
Front Immunol ; 12: 687534, 2021.
Article in English | MEDLINE | ID: covidwho-1295639

ABSTRACT

The clinical significance of antiphospholipid antibodies (aPL) in the context of infections has attracted attention since their first discovery in patients with syphilis. In fact, the recognition of aPL in patients with infections has been described in parallel to the understating of the syndrome. Since the first description of aPL-positive tests in three patients with COVID-19 diagnosed in January 2020 in Wuhan, China, a large number of studies took part in the ongoing debate on SARS-2-Cov 2 induced coagulopathy, and many following reports speculated a potential role for aPL. In order to get further insights on the effective role of detectable aPL in the pro-thrombotic status observed in COVID-19 patients, we performed an observational age-sex controlled study to compare the aPL profile of hospitalized patients with COVID with those observed in a) patients with thrombotic APS and b) patients with cultural/serologically-proved infections. Our data showed positive aPL testing in about half of the patients (53%) with COVID-19 and patients with other viral/bacterial infections (49%). However, aPL profile was different when comparing patients with overt APS and patients with aPL detected in the contest of infections. Caution is therefore required in the interpretation and generalization of the role of aPL s in the management of patients with COVID-19. Before introducing aPL testing as a part of the routine testing in patients with COVID-19, larger well-designed clinical studies are required. While the pro-thrombotic status in patients with COVID-19 is now unquestionable, different mechanisms other than aPL should be further investigated.


Subject(s)
Antibodies, Antiphospholipid/blood , Antiphospholipid Syndrome/pathology , Bacterial Infections/pathology , COVID-19/pathology , Disseminated Intravascular Coagulation/pathology , Virus Diseases/pathology , Aged , Antibodies, Antiphospholipid/immunology , Antiphospholipid Syndrome/complications , Antiphospholipid Syndrome/immunology , Bacterial Infections/complications , COVID-19/complications , COVID-19/immunology , Disseminated Intravascular Coagulation/virology , Female , Humans , Male , SARS-CoV-2/immunology , Virus Diseases/complications
8.
Genes Immun ; 22(3): 141-160, 2021 07.
Article in English | MEDLINE | ID: covidwho-1275909

ABSTRACT

When surveying the current literature on COVID-19, the "cytokine storm" is considered to be pathogenetically involved in its severe outcomes such as acute respiratory distress syndrome, systemic inflammatory response syndrome, and eventually multiple organ failure. In this review, the similar role of DAMPs is addressed, that is, of those molecules, which operate upstream of the inflammatory pathway by activating those cells, which ultimately release the cytokines. Given the still limited reports on their role in COVID-19, the emerging topic is extended to respiratory viral infections with focus on influenza. At first, a brief introduction is given on the function of various classes of activating DAMPs and counterbalancing suppressing DAMPs (SAMPs) in initiating controlled inflammation-promoting and inflammation-resolving defense responses upon infectious and sterile insults. It is stressed that the excessive emission of DAMPs upon severe injury uncovers their fateful property in triggering dysregulated life-threatening hyperinflammatory responses. Such a scenario may happen when the viral load is too high, for example, in the respiratory tract, "forcing" many virus-infected host cells to decide to commit "suicidal" regulated cell death (e.g., necroptosis, pyroptosis) associated with release of large amounts of DAMPs: an important topic of this review. Ironically, although the aim of this "suicidal" cell death is to save and restore organismal homeostasis, the intrinsic release of excessive amounts of DAMPs leads to those dysregulated hyperinflammatory responses-as typically involved in the pathogenesis of acute respiratory distress syndrome and systemic inflammatory response syndrome in respiratory viral infections. Consequently, as briefly outlined in this review, these molecules can be considered valuable diagnostic and prognostic biomarkers to monitor and evaluate the course of the viral disorder, in particular, to grasp the eventual transition precociously from a controlled defense response as observed in mild/moderate cases to a dysregulated life-threatening hyperinflammatory response as seen, for example, in severe/fatal COVID-19. Moreover, the pathogenetic involvement of these molecules qualifies them as relevant future therapeutic targets to prevent severe/ fatal outcomes. Finally, a theory is presented proposing that the superimposition of coronavirus-induced DAMPs with non-virus-induced DAMPs from other origins such as air pollution or high age may contribute to severe and fatal courses of coronavirus pneumonia.


Subject(s)
Alarmins/immunology , COVID-19/immunology , Cytokine Release Syndrome/immunology , Respiratory Distress Syndrome/immunology , SARS-CoV-2/immunology , Virus Diseases/immunology , Alarmins/metabolism , COVID-19/metabolism , COVID-19/virology , Cytokine Release Syndrome/metabolism , Cytokines/immunology , Cytokines/metabolism , Humans , Inflammation/immunology , Inflammation/metabolism , Models, Immunological , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/metabolism , SARS-CoV-2/physiology , Virus Diseases/complications , Virus Diseases/metabolism
9.
Arch Toxicol ; 95(7): 2235-2253, 2021 07.
Article in English | MEDLINE | ID: covidwho-1239455

ABSTRACT

Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease that affects about a quarter of the world population. MAFLD encompasses different disease stadia ranging from isolated liver steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis and hepatocellular carcinoma. Although MAFLD is considered as the hepatic manifestation of the metabolic syndrome, multiple concomitant disease-potentiating factors can accelerate disease progression. Among these risk factors are diet, lifestyle, genetic traits, intake of steatogenic drugs, male gender and particular infections. Although infections often outweigh the development of fatty liver disease, pre-existing MAFLD could be triggered to progress towards more severe disease stadia. These combined disease cases might be underreported because of the high prevalence of both MAFLD and infectious diseases that can promote or exacerbate fatty liver disease development. In this review, we portray the molecular and cellular mechanisms by which the most relevant viral, bacterial and parasitic infections influence the progression of fatty liver disease and steatohepatitis. We focus in particular on how infectious diseases, including coronavirus disease-19, hepatitis C, acquired immunodeficiency syndrome, peptic ulcer and periodontitis, exacerbate MAFLD. We specifically underscore the synergistic effects of these infections with other MAFLD-promoting factors.


Subject(s)
Bacterial Infections/complications , Non-alcoholic Fatty Liver Disease/complications , Parasitic Diseases/complications , Symptom Flare Up , Virus Diseases/complications , Acquired Immunodeficiency Syndrome/complications , Bacterial Infections/microbiology , COVID-19/complications , Hepatitis, Viral, Human/complications , Humans , Liver/physiopathology , Metabolic Syndrome , Non-alcoholic Fatty Liver Disease/microbiology , Non-alcoholic Fatty Liver Disease/parasitology , Non-alcoholic Fatty Liver Disease/virology , Parasitic Diseases/parasitology , Peptic Ulcer , Periodontitis , Risk Factors , Virus Diseases/virology
10.
Biochim Biophys Acta Mol Basis Dis ; 1867(10): 166198, 2021 10 01.
Article in English | MEDLINE | ID: covidwho-1263225

ABSTRACT

Some maternal infections, contracted before or during pregnancy, can be transmitted to the fetus, during gestation (congenital infection), during labor and childbirth (perinatal infection) and through breastfeeding (postnatal infection). The agents responsible for these infections can be viruses, bacteria, protozoa, fungi. Among the viruses most frequently responsible for congenital infections are Cytomegalovirus (CMV), Herpes simplex 1-2, Herpes virus 6, Varicella zoster. Moreover Hepatitis B and C virus, HIV, Parvovirus B19 and non-polio Enteroviruses when contracted during pregnancy may involve the fetus or newborn at birth. Recently, new viruses have emerged, SARS-Cov-2 and Zika virus, of which we do not yet fully know the characteristics and pathogenic power when contracted during pregnancy. Viral infections in pregnancy can damage the fetus (spontaneous abortion, fetal death, intrauterine growth retardation) or the newborn (congenital anomalies, organ diseases with sequelae of different severity). Some risk factors specifically influence the incidence of transmission to the fetus: the timing of the infection in pregnancy, the order of the infection, primary or reinfection or chronic, the duration of membrane rupture, type of delivery, socio-economic conditions and breastfeeding. Frequently infected neonates, symptomatic at birth, have worse outcomes than asymptomatic. Many asymptomatic babies develop long term neurosensory outcomes. The way in which the virus interacts with the maternal immune system, the maternal-fetal interface and the placenta explain these results and also the differences that are observed from time to time in the fetal­neonatal outcomes of maternal infections. The maternal immune system undergoes functional adaptation during pregnancy, once thought as physiological immunosuppression. This adaptation, crucial for generating a balance between maternal immunity and fetus, is necessary to promote and support the pregnancy itself and the growth of the fetus. When this adaptation is upset by the viral infection, the balance is broken, and the infection can spread and lead to the adverse outcomes previously described. In this review we will describe the main viral harmful infections in pregnancy and the potential mechanisms of the damages on the fetus and newborn.


Subject(s)
Congenital Abnormalities/etiology , Infectious Disease Transmission, Vertical , Pregnancy Complications, Infectious , Virus Diseases/complications , Animals , COVID-19/complications , COVID-19/diagnosis , COVID-19/prevention & control , COVID-19/transmission , Congenital Abnormalities/diagnosis , Congenital Abnormalities/prevention & control , Cytomegalovirus/isolation & purification , Cytomegalovirus Infections/complications , Cytomegalovirus Infections/diagnosis , Cytomegalovirus Infections/prevention & control , Cytomegalovirus Infections/transmission , Female , Humans , Pregnancy , Pregnancy Complications, Infectious/diagnosis , Pregnancy Complications, Infectious/prevention & control , Pregnancy Outcome , SARS-CoV-2/isolation & purification , Virus Diseases/diagnosis , Virus Diseases/prevention & control , Virus Diseases/transmission , Zika Virus/isolation & purification , Zika Virus Infection/complications , Zika Virus Infection/diagnosis , Zika Virus Infection/prevention & control , Zika Virus Infection/transmission
11.
Neurosci Biobehav Rev ; 127: 520-530, 2021 08.
Article in English | MEDLINE | ID: covidwho-1228121

ABSTRACT

The historical association between respiratory infections and neuropsychiatric symptoms dates back centuries, with more recent literature highlighting a link between viral infections and schizophrenia. Maternal influenza infection during pregnancy has been associated with the development of schizophrenia in offspring. Viral infections in neonates, children, and adolescents have also been associated with later development of schizophrenia. Neuroinvasive and/or systemic infections are thought to increase risk for psychopathology via inflammatory mechanisms, particularly when exposure occurs during critical neurodevelopmental windows. Several human coronaviruses (HCoVs) have been associated with psychotic disorders and increasing reports of the neuropsychiatric manifestations of COVID-19 suggest it has neuroinvasive properties similar to those of other HCoVs. These properties, in conjunction with its ability to generate a massive inflammatory response, suggest that COVID-19 may also contribute to future psychopathology. This review will summarize the psychopathogenic mechanisms of viral infections and discuss the neuroinvasive and inflammatory properties of COVID-19 that could contribute to the development of psychotic disorders, with a focus on in utero, neonatal, and childhood exposure.


Subject(s)
COVID-19 , Psychotic Disorders , Schizophrenia , Virus Diseases , Adolescent , Child , Female , Humans , Infant, Newborn , Pregnancy , SARS-CoV-2 , Virus Diseases/complications
12.
Curr Opin Neurol ; 34(3): 410-416, 2021 06 01.
Article in English | MEDLINE | ID: covidwho-1153309

ABSTRACT

PURPOSE OF REVIEW: The COVID-19 pandemic has cast increased attention on emerging infections. Clinicians and public health experts should be aware of emerging infectious causes of encephalitis, mechanisms by which they are transmitted, and clinical manifestations of disease. RECENT FINDINGS: A number of arthropod-borne viral infections -- transmitted chiefly by mosquitoes and ticks -- have emerged in recent years to cause outbreaks of encephalitis. Examples include Powassan virus in North America, Chikungunya virus in Central and South America, and tick-borne encephalitis virus in Europe. Many of these viruses exhibit complex life cycles and can infect multiple host animals in addition to humans. Factors thought to influence emergence of these diseases, including changes in climate and land use, are also believed to underlie the emergence of the rickettsial bacterium Orientia tsutsugamushi, now recognized as a major causative agent of acute encephalitis syndrome in South Asia. In addition, the COVID-19 pandemic has highlighted the role of bats as carriers of viruses. Recent studies have begun to uncover mechanisms by which the immune systems of bats are poised to allow for viral tolerance. Several bat-borne infections, including Nipah virus and Ebola virus, have resulted in recent outbreaks of encephalitis. SUMMARY: Infectious causes of encephalitis continue to emerge worldwide, in part because of climate change and human impacts on the environment. Expansion of surveillance measures will be critical in rapid diagnosis and limiting of outbreaks in the future.


Subject(s)
COVID-19/complications , Encephalitis, Arbovirus/transmission , Encephalitis/etiology , Virus Diseases/complications , Animals , Humans , Pandemics , Public Health Surveillance , Virus Diseases/transmission
13.
Int J Mol Sci ; 22(6)2021 Mar 20.
Article in English | MEDLINE | ID: covidwho-1143520

ABSTRACT

The recent pandemic Sars-CoV2 infection and studies on previous influenza epidemic have drawn attention to the association between the obesity and infectious diseases susceptibility and worse outcome. Metabolic complications, nutritional aspects, physical inactivity, and a chronic unbalance in the hormonal and adipocytokine microenvironment are major determinants in the severity of viral infections in obesity. By these pleiotropic mechanisms obesity impairs immune surveillance and the higher leptin concentrations produced by adipose tissue and that characterize obesity substantially contribute to such immune response dysregulation. Indeed, leptin not only controls energy balance and body weight, but also plays a regulatory role in the interplay between energy metabolism and immune system. Since leptin receptor is expressed throughout the immune system, leptin may exert effects on cells of both innate and adaptive immune system. Chronic inflammatory states due to metabolic (i.e., obesity) as well as infectious diseases increase leptin concentrations and consequently lead to leptin resistance further fueling inflammation. Multiple factors, including inflammation and ER stress, contribute to leptin resistance. Thus, if leptin is recognized as one of the adipokines responsible for the low grade inflammation found in obesity, on the other hand, impairments of leptin signaling due to leptin resistance appear to blunt the immunologic effects of leptin and possibly contribute to impaired vaccine-induced immune responses. However, many aspects concerning leptin interactions with inflammation and immune system as well as the therapeutical approaches to overcome leptin resistance and reduced vaccine effectiveness in obesity remain a challenge for future research.


Subject(s)
Leptin/immunology , Leptin/metabolism , Obesity/complications , Obesity/virology , Virus Diseases/complications , Animals , Antiviral Agents/therapeutic use , COVID-19/complications , COVID-19/drug therapy , COVID-19/immunology , COVID-19/metabolism , Energy Metabolism/immunology , Humans , Immune System/metabolism , Immune System/virology , Obesity/immunology , Obesity/metabolism , Viral Vaccines/therapeutic use , Virus Diseases/drug therapy , Virus Diseases/immunology , Virus Diseases/metabolism
14.
Int J Infect Dis ; 105: 617-620, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1101292

ABSTRACT

The global coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in an unprecedented challenge to our healthcare system. Secondary and concurrent bacterial and viral co-infections are well documented for other viral respiratory pathogens; however knowledge regarding co-infections in COVID-19 remains limited. In the present study, concurrent testing of 50 419 individual samples for the presence of SARS-CoV-2 and other bacterial and viral respiratory pathogens was performed between March and August 2020. Overall, a lower rate of viral co-infection was observed in the SARS-CoV-2-positive population when compared to the population testing negative for the virus. Significant levels of Staphylococcus aureus and Epstein-Barr virus co-infections were detected in the SARS-CoV-2-positive population. This is one of the largest surveys looking into the co-infection patterns of SARS-CoV-2 infection in the United States. Data from this study will enhance our understanding of the current pandemic and will assist clinicians in making better patient care decisions, especially with respect to antimicrobial therapy.


Subject(s)
Bacterial Infections/complications , COVID-19/complications , Coinfection , Virus Diseases/complications , Adolescent , Adult , Aged , Aged, 80 and over , Anti-Infective Agents , COVID-19/epidemiology , Child , Child, Preschool , Coinfection/epidemiology , Epstein-Barr Virus Infections/complications , Herpesvirus 4, Human , Humans , Incidence , Infant , Infant, Newborn , Middle Aged , SARS-CoV-2 , Young Adult
15.
Australas J Dermatol ; 62(2): 141-150, 2021 May.
Article in English | MEDLINE | ID: covidwho-1087924

ABSTRACT

In the last few months, there have been numerous reports describing a variety of cutaneous signs associated with COVID-19. Clinicians from Italy were the first to describe the cutaneous manifestations of COVID-19, which were later observed in other parts of the globe. In some cases, cutaneous signs were the only manifestation of COVID-19 rather than the typical syndrome of fever and upper respiratory tract symptoms. However, there is considerable heterogeneity amongst the cutaneous signs described so far, which has been published extensively. Our aim is to summarise the latest studies that have reported the early and late cutaneous signs of COVID-19 and compare them to the most common established viral exanthems.


Subject(s)
COVID-19/complications , Skin Diseases/virology , Humans , SARS-CoV-2 , Virus Diseases/complications
16.
Crit Rev Microbiol ; 47(3): 307-322, 2021 May.
Article in English | MEDLINE | ID: covidwho-1078679

ABSTRACT

The ongoing COVID-19 pandemic has made us wonder what led to its occurrence and what can be done to avoid such events in the future. As we document, one changing circumstance that is resulting in the emergence and changing the expression of viral diseases in both plants and animals is climate change. Of note, the rapidly changing environment and weather conditions such as excessive flooding, droughts, and forest fires have raised concerns about the global ecosystem's security, sustainability, and balance. In this review, we discuss the main consequences of climate change and link these to how they impact the appearance of new viral pathogens, how they may facilitate transmission between usual and novel hosts, and how they may also affect the host's ability to manage the infection. We emphasize how changes in temperature and humidity and other events associated with climate change influence the reservoirs of viral infections, their transmission by insects and other intermediates, their survival outside the host as well the success of infection in plants and animals. We conclude that climate change has mainly detrimental consequences for the emergence, transmission, and outcome of viral infections and plead the case for halting and hopefully reversing this dangerous event.


Subject(s)
COVID-19/transmission , Climate Change , Communicable Diseases, Emerging/transmission , Plant Diseases/virology , Virus Diseases/transmission , Animals , Aquatic Organisms/virology , COVID-19/complications , COVID-19/etiology , COVID-19/immunology , Chiroptera/virology , Communicable Diseases, Emerging/complications , Communicable Diseases, Emerging/etiology , Communicable Diseases, Emerging/immunology , Crops, Agricultural/virology , Disease Reservoirs/virology , Disease Vectors/classification , Food Supply , Humans , Humidity , Plant Diseases/immunology , Primate Diseases/transmission , Primate Diseases/virology , Primates , Rain , Seasons , Temperature , Virus Diseases/complications , Virus Diseases/etiology , Virus Diseases/immunology
17.
Int J Mol Sci ; 22(4)2021 Feb 07.
Article in English | MEDLINE | ID: covidwho-1069828

ABSTRACT

The current pandemic of coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While this respiratory virus only causes mild symptoms in younger healthy individuals, elderly people and those with cardiovascular diseases such as systemic hypertension are susceptible to developing severe conditions that can be fatal. SARS-CoV-2 infection is also associated with an increased incidence of cardiovascular diseases such as myocardial injury, acute coronary syndrome, and thromboembolism. Understanding the mechanisms of the effects of this virus on the cardiovascular system should thus help develop therapeutic strategies to reduce the mortality and morbidity associated with SARS-CoV-2 infection. Since this virus causes severe and fatal conditions in older individuals with cardiovascular comorbidities, effective therapies targeting specific populations will likely contribute to ending this pandemic. In this review article, the effects of various viruses-including other coronaviruses, influenza, dengue, and human immunodeficiency virus-on the cardiovascular system are described to help provide molecular mechanisms of pathologies associated with SARS-CoV-2 infection and COVID-19. The goal is to provide mechanistic information from the biology of other viral infections in relation to cardiovascular pathologies for the purpose of developing improved vaccines and therapeutic agents effective in preventing and/or treating the acute and long-term consequences of SARS-CoV-2 and COVID-19.


Subject(s)
COVID-19/complications , Cardiovascular Diseases/complications , Virus Diseases/complications , Angiotensin-Converting Enzyme 2/metabolism , Animals , COVID-19/metabolism , COVID-19/physiopathology , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/physiopathology , Humans , SARS-CoV-2/physiology , Signal Transduction , Spike Glycoprotein, Coronavirus/metabolism , Virus Diseases/metabolism , Virus Diseases/physiopathology
18.
Sci Rep ; 11(1): 1793, 2021 01 19.
Article in English | MEDLINE | ID: covidwho-1065942

ABSTRACT

COVID-19 caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) and other respiratory viral (non-CoV-2-RV) infections are associated with thrombotic complications. The differences in prothrombotic potential between SARS-CoV-2 and non-CoV-2-RV have not been well characterised. We compared the thrombotic rates between these two groups of patients directly and further delved into their coagulation profiles. In this single-center, retrospective cohort study, all consecutive COVID-19 and non-CoV-2-RV patients admitted between January 15th and April 10th 2020 were included. Coagulation parameters studied were prothrombin time and activated partial thromboplastin time and its associated clot waveform analysis (CWA) parameter, min1, min2 and max2. In the COVID-19 (n = 181) group there were two (1.0 event/1000-hospital-days) myocardial infarction events while one (1.8 event/1000-hospital-day) was reported in the non-CoV-2-RV (n = 165) group. These events occurred in patients who were severely ill. There were no venous thrombotic events. Coagulation parameters did not differ throughout the course of mild COVID-19. However, CWA parameters were significantly higher in severe COVID-19 compared with mild disease, suggesting hypercoagulability (min1: 6.48%/s vs 5.05%/s, P < 0.001; min2: 0.92%/s2 vs 0.74%/s2, P = 0.033). In conclusion, the thrombotic rates were low and did not differ between COVID-19 and non-CoV-2-RV patients. The hypercoagulability in COVID-19 is a highly dynamic process with the highest risk occurring when patients were most severely ill. Such changes in haemostasis could be detected by CWA. In our population, a more individualized thromboprophylaxis approach, considering clinical and laboratory factors, is preferred over universal pharmacological thromboprophylaxis for all hospitalized COVID-19 patients and such personalized approach warrants further research.


Subject(s)
COVID-19/pathology , Thrombophilia/diagnosis , Virus Diseases/pathology , Adult , COVID-19/complications , COVID-19/virology , Female , Humans , Male , Myocardial Infarction/complications , Myocardial Infarction/diagnosis , Partial Thromboplastin Time , Prothrombin Time , Retrospective Studies , Risk Factors , SARS-CoV-2/isolation & purification , Severity of Illness Index , Thrombophilia/complications , Virus Diseases/complications
19.
Int J Mol Sci ; 22(1)2020 Dec 22.
Article in English | MEDLINE | ID: covidwho-1027278

ABSTRACT

Infectious diseases represent a relevant issue in lung cancer patients. Bacterial and viral infections might influence the patients' prognosis, both directly affecting the immune system and indirectly impairing the outcome of anticancer treatments, mainly immunotherapy. In this analysis, we aimed to review the current evidence in order to clarify the complex correlation between infections and lung cancer. In detail, we mainly explored the potential impact on immunotherapy outcome/safety of (1) bacterial infections, with a detailed focus on antibiotics; and (2) viral infections, discriminating among (a) human immune-deficiency virus (HIV), (b) hepatitis B/C virus (HBV-HCV), and (c) Sars-Cov-2. A series of studies suggested the prognostic impact of antibiotic therapy administration, timing, and exposure ratio in patients treated with immune checkpoint inhibitors, probably through an antibiotic-related microbiota dysbiosis. Although cancer patients with HIV, HBV, and HCV were usually excluded from clinical trials evaluating immunotherapy, some retrospective and prospective trials performed in these patient subgroups reported similar results compared to those described in not-infected patients, with a favorable safety profile. Moreover, patients with thoracic cancers are particularly at risk of COVID-19 severe outcomes and mortality. Few reports speculated about the prognostic implications of anticancer therapy, including immunotherapy, in lung cancer patients with concomitant Sars-Cov-2 infection, showing, to date, inconsistent results. The correlation between infectious diseases and immunotherapy remains to be further explored and clarified in the context of dedicated trials. In clinical practice, the accurate and prompt multidisciplinary management of lung cancer patients with infections should be encouraged in order to select the best treatment options for these patients, avoiding unexpected toxicities, while maintaining the anticancer effect.


Subject(s)
Bacterial Infections/complications , COVID-19/complications , Carcinoma, Non-Small-Cell Lung/complications , Carcinoma, Non-Small-Cell Lung/therapy , Immunotherapy , Lung Neoplasms/complications , Lung Neoplasms/therapy , Virus Diseases/complications , Acquired Immunodeficiency Syndrome/complications , Acquired Immunodeficiency Syndrome/immunology , Acquired Immunodeficiency Syndrome/pathology , Acquired Immunodeficiency Syndrome/therapy , Anti-Bacterial Agents/administration & dosage , Bacterial Infections/drug therapy , Bacterial Infections/pathology , COVID-19/drug therapy , COVID-19/pathology , Carcinoma, Non-Small-Cell Lung/microbiology , Carcinoma, Non-Small-Cell Lung/virology , HIV/drug effects , Hepatitis B/complications , Hepatitis B/immunology , Hepatitis B/pathology , Hepatitis C/complications , Hepatitis C/drug therapy , Hepatitis C/pathology , Humans , Immune Checkpoint Inhibitors/therapeutic use , Lung Neoplasms/microbiology , Lung Neoplasms/virology , Microbiota/drug effects , Microbiota/immunology
20.
J Heart Lung Transplant ; 39(4): 379-388, 2020 04.
Article in English | MEDLINE | ID: covidwho-783270

ABSTRACT

BACKGROUND: Respiratory viral infections can increase the risk of chronic lung allograft dysfunction after lung transplantation, but the mechanisms are unknown. In this study, we determined whether symptomatic respiratory viral infections after lung transplantation induce circulating exosomes that contain lung-associated self-antigens and assessed whether these exosomes activate immune responses to self-antigens. METHODS: Serum samples were collected from lung transplant recipients with symptomatic lower- and upper-tract respiratory viral infections and from non-symptomatic stable recipients. Exosomes were isolated via ultracentrifugation; purity was determined using sucrose cushion; and presence of lung self-antigens, 20S proteasome, and viral antigens for rhinovirus, coronavirus, and respiratory syncytial virus were determined using immunoblot. Mice were immunized with circulating exosomes from each group and resulting differential immune responses and lung histology were analyzed. RESULTS: Exosomes containing self-antigens, 20S proteasome, and viral antigens were detected at significantly higher levels (p < 0.05) in serum of recipients with symptomatic respiratory viral infections (n = 35) as compared with stable controls (n = 32). Mice immunized with exosomes from recipients with respiratory viral infections developed immune responses to self-antigens, fibrosis, small airway occlusion, and significant cellular infiltration; mice immunized with exosomes from controls did not (p < 0.05). CONCLUSIONS: Circulating exosomes isolated from lung transplant recipients diagnosed with respiratory viral infections contained lung self-antigens, viral antigens, and 20S proteasome and elicited immune responses to lung self-antigens that resulted in development of chronic lung allograft dysfunction in immunized mice.


Subject(s)
Exosomes/metabolism , Graft Rejection/etiology , Graft Rejection/metabolism , Lung Transplantation/adverse effects , Respiratory Tract Infections/metabolism , Virus Diseases/metabolism , Aged , Animals , Antigens, Viral/metabolism , Autoantigens/metabolism , Case-Control Studies , Female , HLA Antigens/metabolism , Humans , Male , Mice , Mice, Inbred C57BL , Middle Aged , Proteasome Endopeptidase Complex/metabolism , Respiratory Tract Infections/complications , Respiratory Tract Infections/virology , Virus Diseases/complications
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