3. Kill or be killed

2018 ◽  
pp. 24-32
Author(s):  
Dorothy H. Crawford
Keyword(s):  
Immune Response ◽  
Herpes Simplex ◽  
The Body ◽  
Protective Mechanism ◽  
Human Immune Response ◽  
Human Immune ◽  
Epstein Barr ◽  
Living Organisms ◽  
Simplex Virus

‘Kill or be killed’ shows how viruses survive—they must reproduce before the host either dies or its immune system recognizes and eliminates them. The transmission routes of viruses such as flu, measles, common cold, herpes simplex virus, HIV, Epstein–Barr, and hepatitis B are discussed. How do we fight viruses? All living organisms have defences against invading viruses. Vertebrates, and possibly some invertebrates, are immune to re-infection by the same virus. Another protective mechanism, used by plants, but also by insects and other animal species, is gene silencing by RNA interference. The human immune response is explained, discussing the role of lymphocytes and immunopathology, where the immune response may actually harm the body.

scholarly journals MORC3, a Component of PML Nuclear Bodies, Has a Role in Restricting Herpes Simplex Virus 1 and Human Cytomegalovirus

2016 ◽  
Vol 90 (19) ◽  
pp. 8621-8633 ◽  
Author(s):  
Elizabeth Sloan ◽  
Anne Orr ◽  
Roger D. Everett
Keyword(s):  
Immune Response ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Hcmv Infection ◽  
Nuclear Bodies ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus ◽  
Antiviral Role ◽  
Hsv 1

ABSTRACTWe previously reported that MORC3, a protein associated with promyelocytic leukemia nuclear bodies (PML NBs), is a target of herpes simplex virus 1 (HSV-1) ICP0-mediated degradation (E. Sloan, et al., PLoS Pathog11:e1005059, 2015,http://dx.doi.org/10.1371/journal.ppat.1005059). Since it is well known that certain other components of the PML NB complex play an important role during an intrinsic immune response to HSV-1 and are also degraded or inactivated by ICP0, here we further investigate the role of MORC3 during HSV-1 infection. We demonstrate that MORC3 has antiviral activity during HSV-1 infection and that this antiviral role is counteracted by ICP0. In addition, MORC3's antiviral role extends to wild-type (wt) human cytomegalovirus (HCMV) infection, as its plaque-forming efficiency increased in MORC3-depleted cells. We found that MORC3 is recruited to sites associated with HSV-1 genomes after their entry into the nucleus of an infected cell, and in wt infections this is followed by its association with ICP0 foci prior to its degradation. The RING finger domain of ICP0 was required for degradation of MORC3, and we confirmed that no other HSV-1 protein is required for the loss of MORC3. We also found that MORC3 is required for fully efficient recruitment of PML, Sp100, hDaxx, and γH2AX to sites associated with HSV-1 genomes entering the host cell nucleus. This study further unravels the intricate ways in which HSV-1 has evolved to counteract the host immune response and reveals a novel function for MORC3 during the host intrinsic immune response.IMPORTANCEHerpesviruses have devised ways to manipulate the host intrinsic immune response to promote their own survival and persistence within the human population. One way in which this is achieved is through degradation or functional inactivation of PML NB proteins, which are recruited to viral genomes in order to repress viral transcription. Because MORC3 associates with PML NBs in uninfected cells and is a target for HSV-1-mediated degradation, we investigated the role of MORC3 during HSV-1 infection. We found that MORC3 is also recruited to viral HSV-1 genomes, and importantly it contributes to the fully efficient recruitment of PML, hDaxx, Sp100, and γH2AX to these sites. Depletion of MORC3 resulted in an increase in ICP0-null HSV-1 and wt HCMV replication and plaque formation; therefore, this study reveals that MORC3 is an antiviral factor which plays an important role during HSV-1 and HCMV infection.

Human immune response in schistosomiasis: the role of P24 in the modulation of cellular reactivity to Schistosoma mansoni antigens

2002 ◽  
Vol 63 (8) ◽  
pp. 647-656 ◽  
Author(s):  
C.láudia Soares Zouain ◽  
Shauma Gustavson ◽  
David Nascimento Silva-Teixeira ◽  
Christiane Contigli ◽  
Virmondes Rodrigues ◽  
...  
Keyword(s):  
Immune Response ◽  
Schistosoma Mansoni ◽  
Human Immune Response ◽  
Human Immune

scholarly journals T Cell-Derived Lymphotoxin Is Essential for the Anti-Herpes Simplex Virus 1 Humoral Immune Response

2018 ◽  
Vol 92 (14) ◽  
Author(s):  
Kaiting Yang ◽  
Yong Liang ◽  
Zhichen Sun ◽  
Diyuan Xue ◽  
Hairong Xu ◽  
...  
Keyword(s):  
Immune Response ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Humoral Immune Response ◽  
Herpes Simplex Virus 1 ◽  
Humoral Immune ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTB cell-derived lymphotoxin (LT) is required for the development of follicular dendritic cell clusters for the formation of primary and secondary lymphoid follicles, but the role of T cell-derived LT in antibody response has not been well demonstrated. We observed that lymphotoxin β-receptor (LTβR) signaling is essential for optimal humoral immune response and protection against an acute herpes simplex virus 1 (HSV-1) infection. Blocking the LTβR pathway caused poor maintenance of germinal center B (GC-B) cells and follicular helper T (Tfh) cells. Using bone marrow chimeric mice and adoptive transplantation, we determined that T cell-derived LT played an indispensable role in the humoral immune response to HSV-1. Upregulation of gamma interferon by the LTβR-Ig blockade impairs the sustainability of Tfh-like cells, leading to an impaired humoral immune response. Our findings have identified a novel role of T cell-derived LT in the humoral immune response against HSV-1 infection.IMPORTANCEImmunocompromised people are susceptible to HSV-1 infection and lethal recurrence, which could be inhibited by anti-HSV-1 humoral immune response in the host. This study sought to explore the role of T cell-derived LT in the anti-HSV-1 humoral immune response using LT-LTβR signaling-deficient mice and the LTβR-Ig blockade. The data indicate that the T cell-derived LT may play an essential role in sustaining Tfh-like cells and ensure Tfh-like cells' migration into primary or secondary follicles for further maturation. This study provides insights for vaccine development against infectious diseases.

scholarly journals ROLE OF INFECTION IN THE ORIGIN, COURSE, RESULTS OF TREATMENT OF TOXIC GOITER

2020 ◽  
Vol 23 (2) ◽  
pp. 195-200
Author(s):  
I. V. Tereshchenko
Keyword(s):  
Herpes Simplex ◽  
Viral Infections ◽  
Autoimmune Process ◽  
Results Of Treatment ◽  
Acute Infections ◽  
Epstein Barr ◽  
Combined Infection ◽  
Simplex Virus ◽  
Toxic Goiter

To date, the question of the causes of toxic goiter has not been resolved. Purpose: to analyze the role of infection in the occurrence, course, treatment outcome of toxic goiter. Observed in the dynamics of 64 patients with toxic goiter. In 36% of cases, thyrotoxicosis manifested itself after acute infections. Foci of chronic bacterial infection were detected in 59 (92.2%) patients. Serological indices of persistence of herpes simplex virus, Epstein- Barr, cytomegalovirus (HSV, EBV, CMV) were high in all patients with suspected viral persistence (n = 20). In 1/3 of the observations a combined infection was established. The infection was cured in 34 patients. The infection was not cured in 30 patients. The observations showed that acute and chronic bacterial and viral infections can provoke the onset of toxic goiter, worsen its course, reduce the effectiveness of therapy, affecting the main link in the pathogenesis of the disease - the activity of the autoimmune process in the thyroid gland. Infection exacerbations stimulate the production of AT-rTTG, leading to relapses thyrotoxicosis. Conclusion: although infection is not the main etiological factor of toxic goiter, its role in the manifestation, course of toxic goiter, the effectiveness of therapy, and the distant prognosis is undeniable. Starting treatment for toxic goiter, in including planning surgical treatment or radioiodine therapy, it is necessary to identify and sanitize foci of infection, to check the possible persistence of common viruses of herpes simplex, Epstein-Barr, cytomegalovirus. This will improve the prognosis, reduce the high risks of thyrotoxicosis relapses.

scholarly journals Genetics and Molecular Biology of Epstein-Barr Virus-Encoded BART MicroRNA: A Paradigm for Viral Modulation of Host Immune Response Genes and Genome Stability

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
David H. Dreyfus
Keyword(s):  
Immune Response ◽  
Genome Stability ◽  
Epstein Barr Virus ◽  
Host Immune Response ◽  
Barr Virus ◽  
Immune Response Genes ◽  
Human Immune Response ◽  
Human Immune ◽  
Bystander Cells ◽  
Epstein Barr

Epstein-Barr virus, a ubiquitous human herpesvirus, is associated through epidemiologic evidence with common autoimmune syndromes and cancers. However, specific genetic mechanisms of pathogenesis have been difficult to identify. In this review, the author summarizes evidence that recently discovered noncoding RNAs termed microRNA encoded by Epstein-Barr virus BARF (BamHI A right frame) termed BART (BamHI A right transcripts) are modulators of human immune response genes and genome stability in infected and bystander cells. BART expression is apparently regulated by complex feedback loops with the host immune response regulatory NF-κB transcription factors. EBV-encoded BZLF-1 (ZEBRA) protein could also regulate BART since ZEBRA contains a terminal region similar to ankyrin proteins such as IκBαthat regulate host NF-κB. BALF-2 (BamHI A left frame transcript), a viral homologue of the immunoglobulin and T cell receptor gene recombinase RAG-1 (recombination-activating gene-1), may also be coregulated with BART since BALF-2 regulatory sequences are located near the BART locus. Viral-encoded microRNA and viral mRNA transferred to bystander cells through vesicles, defective viral particles, or other mechanisms suggest a new paradigm in which bystander or hit-and-run mechanisms enable the virus to transiently or chronically alter human immune response genes as well as the stability of the human genome.

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