Pemphigus Vulgaris Following Influenza: A Case Report

Viruses have long been implicated as potential triggers of autoimmune disease. In the case of pemphigus vulgaris, members of the herpesviridae family are often associated with its development. There have also been reports of pemphigus being triggered by the influenza vaccine. We report a case of a 17-year-old male who developed mucous membrane-predominant pemphigus vulgaris after testing positive for the influenza virus and discuss proposed hypotheses for the association between viral infections and autoimmunity, such as molecular mimicry and epitope spreading.

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Viral Infections and Autoimmune Disease: Roles of LCMV in Delineating Mechanisms of Immune Tolerance

Viruses ◽

10.3390/v11100885 ◽

2019 ◽

Vol 11 (10) ◽

pp. 885

Author(s):

Georgia Fousteri ◽

Amy Dave Jhatakia

Keyword(s):

Immune System ◽

Autoimmune Disease ◽

Viral Infections ◽

Molecular Mimicry ◽

Short Review ◽

Organ Damage ◽

Lymphocytic Choriomeningitis ◽

Immune Deviation ◽

Viral Pathogen ◽

Lcmv Infection

Viral infections are a natural part of our existence. They can affect us in many ways that are the result of the interaction between the viral pathogen and our immune system. Most times, the resulting immune response is beneficial for the host. The pathogen is cleared, thus protecting our vital organs with no other consequences. Conversely, the reaction of our immune system against the pathogen can cause organ damage (immunopathology) or lead to autoimmune disease. To date, there are several mechanisms for virus-induced autoimmune disease, including molecular mimicry and bystander activation, in support of the “fertile field” hypothesis (terms defined in our review). In contrast, viral infections have been associated with protection from autoimmunity through mechanisms that include Treg invigoration and immune deviation, in support of the “hygiene hypothesis”, also defined here. Infection with lymphocytic choriomeningitis virus (LCMV) is one of the prototypes showing that the interaction of our immune system with viruses can either accelerate or prevent autoimmunity. Studies using mouse models of LCMV have helped conceive and establish several concepts that we now know and use to explain how viruses can lead to autoimmune activation or induce tolerance. Some of the most important mechanisms established during the course of LCMV infection are described in this short review.

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Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms

Viruses ◽

10.3390/v11080762 ◽

2019 ◽

Vol 11 (8) ◽

pp. 762 ◽

Cited By ~ 38

Author(s):

Maria K. Smatti ◽

Farhan S. Cyprian ◽

Gheyath K. Nasrallah ◽

Asmaa A. Al Thani ◽

Ruba O. Almishal ◽

...

Keyword(s):

Immune Responses ◽

Autoimmune Diseases ◽

Lupus Erythematosus ◽

Influenza A ◽

Molecular Mechanisms ◽

Viral Infections ◽

Molecular Mimicry ◽

Experimental Studies ◽

Onset Time ◽

Protective Effects

For a long time, viruses have been shown to modify the clinical picture of several autoimmune diseases, including type 1 diabetes (T1D), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome (SS), herpetic stromal keratitis (HSK), celiac disease (CD), and multiple sclerosis (MS). Best examples of viral infections that have been proposed to modulate the induction and development of autoimmune diseases are the infections with enteric viruses such as Coxsackie B virus (CVB) and rotavirus, as well as influenza A viruses (IAV), and herpesviruses. Other viruses that have been studied in this context include, measles, mumps, and rubella. Epidemiological studies in humans and experimental studies in animal have shown that viral infections can induce or protect from autoimmunopathologies depending on several factors including genetic background, host-elicited immune responses, type of virus strain, viral load, and the onset time of infection. Still, data delineating the clear mechanistic interaction between the virus and the immune system to induce autoreactivity are scarce. Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena. Therefore, a better understanding of the immune-related molecular processes in virus-induced autoimmunity is warranted. Here we provide an overview of the current understanding of viral-induced autoimmunity and the mechanisms that are associated with this phenomenon.

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Caffeoylquinic Acids Are Major Constituents with Potent Anti-Influenza Effects in Brazilian Green Propolis Water Extract

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2011/254914 ◽

2011 ◽

Vol 2011 ◽

pp. 1-7 ◽

Cited By ~ 16

Author(s):

Tomohiko Urushisaki ◽

Tomoaki Takemura ◽

Shigemi Tazawa ◽

Mayuko Fukuoka ◽

Junji Hosokawa-Muto ◽

...

Keyword(s):

Influenza Virus ◽

Influenza A ◽

Viral Infections ◽

Influenza Virus Infection ◽

Water Extract ◽

H1n1 Influenza ◽

Caffeoylquinic Acids ◽

Cytoprotective Activity ◽

Infected Cells ◽

Brazilian Green Propolis

Influenza A viral infections reached pandemic levels in 1918, 1957, 1968, and, most recently, in 2009 with the emergence of the swine-origin H1N1 influenza virus. The development of novel therapeutics or prophylactics for influenza virus infection is urgently needed. We examined the evaluation of the anti-influenza virus (A/WSN/33 (H1N1)) activity of Brazilian green propolis water extract (PWE) and its constituents by cell viability and real-time PCR assays. Our findings showed strong evidence that PWE has an anti-influenza effect and demonstrate that caffeoylquinic acids are the active anti-influenza components of PWE. Furthermore, we have found that the amount of viral RNA per cell remained unchanged even in the presence of PWE, suggesting that PWE has no direct impact on the influenza virus but may have a cytoprotective activity by affecting internal cellular process. These findings indicate that caffeoylquinic acids are the active anti-influenza components of PWE. Above findings might facilitate the prophylactic application of natural products and the realization of novel anti-influenza drugs based on caffeoylquinic acids, as well as further the understanding of cytoprotective intracellular mechanisms in influenza virus-infected cells.

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Autoimmune neutropenia associated with influenza virus infection in childhood: a case report

BMC Infectious Diseases ◽

10.1186/s12879-021-06506-9 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Ignacio Callejas Caballero ◽

Marta Illán Ramos ◽

Arantxa Berzosa Sánchez ◽

Eduardo Anguita ◽

José Tomás Ramos Amador

Keyword(s):

Influenza Virus ◽

Influenza A ◽

Viral Infections ◽

Influenza Infection ◽

Influenza Virus Infection ◽

Rapid Test ◽

Male Infant ◽

Severe Neutropenia ◽

Autoimmune Neutropenia ◽

Benign Condition

Abstract Background Although neutropenia is relatively frequent in infants and children and is mostly a benign condition with a self-limited course, it can lead to life-threatening severe infections. Autoimmune neutropenia is a relatively uncommon hematological disorder characterized by the autoantibody-induced destruction of neutrophils. It is usually triggered by viral infections with very few documented cases after influenza virus. Case presentation An 8-month-old male infant presented at the emergency room with a 5-days history of fever up to 39.7 °C, cough and runny nose. In the blood test performed, severe neutropenia was diagnosed (neutrophils 109/μL). A nasopharyngeal aspirate revealed a positive rapid test for Influenza A. Serum antineutrophil antibodies were determined with positive results. Neutropenia targeted panel showed no mutations. Despite maintenance of severe neutropenia for 9 months the course was uneventful without treatment. Conclusions When severe neutropenia is diagnosed and confirmed, it is essential to rule out some potential etiologies and underlying conditions, since the appropriate subsequent management will depend on it. Although autoimmune neutropenia triggered by viral infections has been widely reported, it has seldom been reported after influenza infection. The benign course of the disease allows a conservative management in most cases.

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Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease

Clinical Microbiology Reviews ◽

10.1128/cmr.19.1.80-94.2006 ◽

2006 ◽

Vol 19 (1) ◽

pp. 80-94 ◽

Cited By ~ 302

Author(s):

Robert S. Fujinami ◽

Matthias G. von Herrath ◽

Urs Christen ◽

J. Lindsay Whitton

Keyword(s):

Multiple Sclerosis ◽

Autoimmune Disease ◽

Virus Infection ◽

Molecular Mimicry ◽

Viral Persistence ◽

Target Organ ◽

Virus Infections ◽

Epitope Spreading ◽

Bystander Activation ◽

The Brain

SUMMARY Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistance. These mechanisms have been used separately or in various combinations to account for the immunopathology observed at the site of infection and/or sites of autoimmune disease, such as the brain, heart, and pancreas. These mechanisms are discussed in the context of multiple sclerosis, myocarditis, and diabetes, three immune-medicated diseases often linked with virus infections.

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Early estimates of the effectiveness of the 2011/12 influenza vaccine in the population targeted for vaccination in Spain, 25 December 2011 to 19 February 2012

Eurosurveillance ◽

10.2807/ese.17.12.20129-en ◽

2012 ◽

Vol 17 (12) ◽

Author(s):

S Jiménez-Jorge ◽

S de Mateo ◽

F Pozo ◽

I Casas ◽

M García Cenoz ◽

...

Keyword(s):

Influenza Virus ◽

Influenza Vaccine ◽

Protective Effect ◽

Influenza A ◽

Vaccine Effectiveness ◽

H3n2 Virus ◽

Influenza Epidemic

We present early estimates of influenza vaccine effectiveness (VE) in the population targeted for vaccination, during 25 December 2011 to 19 February 2012. The adjusted VE was 55% (95% CI: 3 to 79) against any type of influenza virus and 54% (95% CI: 1 to 79) against influenza A(H3N2) virus. This suggests a moderate protective effect of the vaccine in the targeted population in a late influenza epidemic with limited match between vaccine and circulating strains.

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Viral Infections and Autoimmune Disease: Roles of LCMV in Delineating Mechanisms of Immune Tolerance

10.20944/preprints201907.0134.v2 ◽

2019 ◽

Author(s):

Georgia Fousteri ◽

Amy Dave Jhatakia

Keyword(s):

Immune System ◽

Autoimmune Disease ◽

Viral Infections ◽

Molecular Mimicry ◽

Short Review ◽

Hygiene Hypothesis ◽

Organ Damage ◽

Lymphocytic Choriomeningitis ◽

Immune Deviation ◽

Viral Pathogen

Viral infections are a natural part of our existence. They can affect us in many ways that are the result of the interaction between the viral pathogen and our immune system. Most times the resulting immune response is beneficial for the host. The pathogen gets cleared thus protecting our vital organs with no other consequences. Conversely, the reaction of our immune system against the pathogen can cause organ damage (immunopathology) or lead to autoimmune disease. To date, there are several mechanisms for virus-induced autoimmune disease, including molecular mimicry and bystander activation, in support of the “fertile field” hypothesis, terms defined in our review. On the flip side, viral infections have been associated with protection from autoimmunity through mechanisms that include Treg invigoration and immune deviation, in support of the “hygiene hypothesis”, also defined here. Infection with lymphocytic choriomeningitis virus (LCMV) is one of the prototypes showing that the interaction of our immune system with viruses can either accelerate or prevent autoimmunity. Studies using mouse models of LCMV have helped conceive and establish several concepts that we today know and explain how viruses can lead to autoimmune activation or induce tolerance. Some of the most important mechanisms established during the course LCMV are described in this short review.

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The p150 Isoform of ADAR1 Blocks Sustained RLR signaling and Apoptosis during Influenza Virus Infection

10.1101/2020.05.23.111419 ◽

2020 ◽

Author(s):

Olivia A. Vogel ◽

Julianna Han ◽

Chieh-Yu Liang ◽

Santhakumar Manicassamy ◽

Jasmine T. Perez ◽

...

Keyword(s):

Influenza Virus ◽

Retinoic Acid ◽

Rna Editing ◽

Influenza A ◽

Viral Infections ◽

Influenza Virus Infection ◽

Negative Regulators ◽

Editing Activity ◽

Editing Enzyme ◽

Inducible Gene

AbstractSignaling through retinoic acid inducible gene I (RIG-I) like receptors (RLRs) is tightly regulated, with activation occurring upon sensing of viral nucleic acids, and suppression mediated by negative regulators. Under homeostatic conditions aberrant activation of melanoma differentiation-associated protein-5 (MDA5) is prevented through editing of endogenous dsRNA by RNA editing enzyme Adenosine Deaminase Acting on RNA (ADAR1). In addition, ADAR1 is postulated to play proviral and antiviral roles during viral infections that are dependent or independent of RNA editing activity. Here, we investigated the importance of ADAR1 isoforms in modulating influenza A virus (IAV) replication and revealed the opposing roles for ADAR1 isoforms, with the nuclear p110 isoform restricting versus the cytoplasmic p150 isoform promoting IAV replication. Importantly, we demonstrate that p150 is critical for preventing sustained RIG-I signaling, as p150 deficient cells showed increased IFN-β expression and apoptosis during IAV infection, independent of RNA editing activity. Taken together, the p150 isoform of ADAR1 is important for preventing sustained RIG-I induced IFN-β expression and apoptosis during viral infection.

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Management of Pemphigus Vulgaris in Pregnancy - Case Report

Journal of Gynecology & Reproductive Medicine ◽

10.33140/jgrm.03.04.01 ◽

2019 ◽

Vol 3 (4) ◽

Keyword(s):

Case Report ◽

Autoimmune Disease ◽

Pemphigus Vulgaris ◽

Clinical Findings ◽

Moderate Intensity ◽

Primary Target ◽

Bullous Disease ◽

Autoimmune Bullous Disease ◽

Homophilic Adhesion ◽

In Pregnancy

Pemphigus vulgaris is a rare autoimmune bullous disease caused by producing autoantibodies directed against transmembrane glycoproteins of desmosomes that can lead to steric hindrance to homophilic adhesion of desmogleins. The development of pemphigus during the pregnancy is rare. The disruption of the Th1:Th2 balance in the autoimmune disease during the pregnancy plays a crucial role and explains why some studies have reported the exacerbation of disease, while others observe improvements during the pregnancy. We present aclinical case of a 31-year-oldprimigravida, with dichorionic - diamniotic twin pregnancyassociatedwith pemphigus vulgaris, being discovered 2 years ago, who went under treatment with Medrol 64mg/day and Imuran 50mg/day. She was admitted to the hospital at 31 weeks of gestation with non-systemic contractions of moderate intensity. The clinical findings are multiple erosions and blisters which have been accentuated during the second semester and have been remitted after delivery. Nowadays, the therapeutic management of the pemphigus during the pregnancy is not yet established and all of these cases are individual evaluated with the primary target to control the disease with the safety of the fetus.

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Madin Darby canine kidney cell-lines used in influenza virus production has resulted in canine 28s being integrated in the influenza virus genome - evidence from Influenza A patients in Hong Kong

10.31219/osf.io/wsry4 ◽

2020 ◽

Author(s):

Sandeep Chakraborty

Keyword(s):

Influenza Virus ◽

Hong Kong ◽

Influenza Vaccine ◽

Mdck Cell ◽

Influenza A ◽

Mdck Cells ◽

Virus Genome ◽

Kidney Cells ◽

Darby Canine Kidney ◽

Canine Kidney

In 1989, 54 nucleotides from chicken 18s were seen to be inserted into the haemagglutinin gene of an influenza virus increasing viral pathogenicity [1]. Previously, I have reported human 18s sequences (from sequence vectors) appended to the influenza virus genome in Covid19 patients from Wuhan and Hong Kong [2]. These human ribosomal sequences are supposed to increase the transcription of the virus in the human cell, and thus will be more pathogenic. Here, I report the circulation of Influenza A genomes with 28s from canine integrated, showing that the escape of lab-made viruses is quite prevalent.Canine 28s sequence appended to flu genomesA recent (2020,Accid:PRJNA605947) study from the University of Hong Kong that did Nanopore sequencing to find novel targets for detection and surveillance of Influenza A viruses [3] shows the integration of canine 28s (Fig 1) sequence to the flu genome. The full read (SRR11067307.3179,SI:fullread.fa) splits into the flu virus (1-1605, SI:flu.baltimore.fa,(Baltimore/R0197/2017(H1N1)) nucleocapsid protein (NP) gene) and canine 28 (1606-1973, SI:canine.28s.fa Accid:XR 004817748.1, Canis lupus dingo 28S)). There is no reason to find canine 28s in clinical samples, barring the fact that canine kidney cells are used to manufacture the virus for several applications, including vaccines.Madin Darby canine kidney cells (MDCK) - why MDCK?The advantages of using MDCK influenza production is well known [4]. MDCK is better in the replication of live attenuated influenza viruses than most other cell lines (like Vero), thus yielding more virus in large-scale production of influenza virus [5]. The virus replicates rapidly in MDCK to ‘produce high titers in MDCK cells in as few as 3 to 10 passages, i.e., in 10–30 days’ [4]. Also, MDCK cells are also good for the production of certain influenza B virus vaccines, and MDCK cell-derived components are not allergenic [6]. Vaccines made using MDCK cellsInfluvac, a split virus vaccine produced in adherent MDCK cells, in the Netherlands in 1999 [7]. The use of MDCK cells (MedImmune) for production of live attenuated influenza vaccine in both serum containing and serum-free media was found to be more efficient [8]. Another trivalent MDCK cell culture-derived influenza vaccine is Optaflu [9]. ”Flucelvax Quadrivalent is the only cell-based inactivated flu vaccine that has been licensed by the FDA for use in the United States.” (https://www.cdc.gov/flu/prevent/cell-based.htm)

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