scholarly journals Hide and Seek: The Interplay Between Zika Virus and the Host Immune Response

2021 ◽  
Vol 12 ◽  
Author(s):  
Lim Jack Lee ◽  
Thamil Vaani Komarasamy ◽  
Nur Amelia Azreen Adnan ◽  
William James ◽  
Vinod RMT Balasubramaniam
Keyword(s):  
Immune Response ◽  
Zika Virus ◽  
Large Scale ◽  
Vaccine Development ◽  
Sexual Transmission ◽  
Adaptive Immune Response ◽  
Host Immune Response ◽  
Interferon Response ◽  
Current Status ◽  
Successful Infection

Zika virus (ZIKV) received worldwide attention over the past decade when outbreaks of the disease were found to be associated with severe neurological syndromes and congenital abnormalities. Unlike most other flaviviruses, ZIKV can spread through sexual and transplacental transmission, adding to the complexity of Zika pathogenesis and clinical outcomes. In addition, the spread of ZIKV in flavivirus-endemic regions, and the high degree of structural and sequence homology between Zika and its close cousin Dengue have raised questions on the interplay between ZIKV and the pre-existing immunity to other flaviviruses and the potential immunopathogenesis. The Zika epidemic peaked in 2016 and has affected over 80 countries worldwide. The re-emergence of large-scale outbreaks in the future is certainly a possibility. To date, there has been no approved antiviral or vaccine against the ZIKV. Therefore, continuing Zika research and developing an effective antiviral and vaccine is essential to prepare the world for a future Zika epidemic. For this purpose, an in-depth understanding of ZIKV interaction with many different pathways in the human host and how it exploits the host immune response is required. For successful infection, the virus has developed elaborate mechanisms to escape the host response, including blocking host interferon response and shutdown of certain host cell translation. This review provides a summary on the key host factors that facilitate ZIKV entry and replication and the mechanisms by which ZIKV antagonizes antiviral innate immune response and involvement of adaptive immune response leading to immunopathology. We also discuss how ZIKV modulates the host immune response during sexual transmission and pregnancy to induce infection, how the cross-reactive immunity from other flaviviruses impacts ZIKV infection, and provide an update on the current status of ZIKV vaccine development.

scholarly journals Evolution of the innate and adaptive immune response in women with acute Zika virus infection

2019 ◽  
Vol 5 (1) ◽  
pp. 76-83 ◽  
Author(s):  
Pierre Tonnerre ◽  
Juliana G. Melgaço ◽  
Almudena Torres-Cornejo ◽  
Marcelo A. Pinto ◽  
Constanze Yue ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Zika Virus ◽  
Adaptive Immune Response ◽  
Adaptive Immune ◽  
Zika Virus Infection

RNA sensors as a mechanism of innate immune evasion among SARS-CoV2, HIV and Nipah viruses

2021 ◽  
Vol 22 ◽  
Author(s):  
Dalia Cicily Kattiparambil Dixon ◽  
Chameli Ratan ◽  
Bhagyalakshmi Nair ◽  
Sabitha Mangalath ◽  
Rachy Abraham ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Innate Immune Response ◽  
Vaccine Development ◽  
Innate Immune ◽  
Interferon Response ◽  
Host Immune System ◽  
Type I ◽  
Adaptive Responses ◽  
Rna Sensors

: Innate immunity is the first line of defence elicited by the host immune system to fight against invading pathogens such as viruses and bacteria. From this elementary immune response, the more complex antigen-specific adaptive responses are recruited to provide a long-lasting memory against the pathogens. Innate immunity gets activated when the host cell utilizes a diverse set of receptors known as pattern recognition receptors (PRR) to recognize the viruses that have penetrated the host and respond with cellular processes like complement system, phagocytosis, cytokine release and inflammation and destruction of NK cells. Viral RNA or DNA or viral intermediate products are recognized by receptors like toll-like receptors(TLRs), nucleotide oligomerization domain(NOD)-like receptors (NLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) thereby, inducing type I interferon response (IFN) and other proinflammatory cytokines in infected cells or other immune cells. But certain viruses can evade the host innate immune response to replicate efficiently, triggering the spread of the viral infection. The present review describes the similarity in the mechanism chosen by viruses from different families -HIV, SARS-CoV2 and Nipah viruses to evade the innate immune response and how efficiently they establish the infection in the host. The review also addresses the stages of developments of various vaccines against these viral diseases and the challenges encountered by the researchers during vaccine development.

scholarly journals Development of vaccines against the sexually transmitted infections gonorrhoea, syphilis, Chlamydia, herpes simplex virus, human immunodeficiency virus and Zika virus

2020 ◽  
Vol 8 ◽  
pp. 251513552092388
Author(s):  
Edwin David G. McIntosh
Keyword(s):  
Human Immunodeficiency Virus ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Sexually Transmitted Infections ◽  
Zika Virus ◽  
Vaccine Development ◽  
Current Status ◽  
Sexually Transmitted ◽  
Immunodeficiency Virus ◽  
Simplex Virus

The success in preventing hepatitis B virus and human papillomavirus infections by means of vaccination paves the way for the development of other vaccines to prevent sexually transmitted infections (STIs) such as gonorrhoea, syphilis, chlamydia, herpes simplex virus, human immunodeficiency virus and Zika virus. The current status of vaccine development for these infections will be explored in this review. The general principles for success include the need for prevention of latency, persistence and repeat infections. A reduction in transmission of STIs would reduce the global burden of disease. Therapeutic activity of vaccines against STIs would be advantageous over preventative activity alone, and prevention of congenital and neonatal infections would be an added benefit. There would be an added value in the prevention of long-term consequences of STIs. It may be possible to re-purpose ‘old’ vaccines for new indications. One of the major challenges is the determination of the target populations for STI vaccination.

scholarly journals Hypercholesterolemia Impairs Immunity to Tuberculosis

2008 ◽  
Vol 76 (8) ◽  
pp. 3464-3472 ◽  
Author(s):  
Gregory W. Martens ◽  
Meltem Cevik Arikan ◽  
Jinhee Lee ◽  
Fucheng Ren ◽  
Therese Vallerskog ◽  
...  
Keyword(s):  
Immune Response ◽  
Ex Vivo ◽  
Bacterial Load ◽  
Elevated Serum ◽  
Adaptive Immune Response ◽  
Interferon Response ◽  
Lung Pathology ◽  
Inflammatory Cytokine Production ◽  
Adaptive Immune ◽  
Elevated Serum Cholesterol

ABSTRACT We demonstrate that apolipoprotein E -deficient (ApoE −/ −) mice are highly susceptible to tuberculosis and that their susceptibility depends on the severity of hypercholesterolemia. Wild-type (WT) mice and ApoE −/ − mice fed a low-cholesterol (LC) or high-cholesterol (HC) diet were infected with ∼50 CFU Mycobacterium tuberculosis Erdman by aerosol. ApoE −/ − LC mice were modestly more susceptible to tuberculosis than WT LC mice. In contrast, ApoE −/ − HC mice were extremely susceptible, as evidenced by 100% mortality after 4 weeks with tuberculosis. The lung pathology of ApoE −/ − HC mice was remarkable for giant abscess-like lesions, massive infiltration by granulocytes, elevated inflammatory cytokine production, and a mean bacterial load ∼2 log units higher than that of WT HC mice. Compared to WT HC mice, the gamma interferon response of splenocytes restimulated ex vivo with M. tuberculosis culture filtrate protein was delayed in ApoE −/ − HC mice, and they failed to control M. tuberculosis growth in the lung. OT-II cells adoptively transferred into uninfected ApoE −/ − HC mice had a weak proliferative response to their antigen, indicating impaired priming of the adaptive immune response. Our studies show that ApoE −/ − deficiency is associated with delayed expression of adaptive immunity to tuberculosis caused by defective priming of the adaptive immune response and that elevated serum cholesterol is responsible for this effect.

scholarly journals Inverse Vaccination to Silence Immunity to Myelin in Multiple Sclerosis

2010 ◽  
Vol 37 (S2) ◽  
pp. S49-S58 ◽  
Author(s):  
Lawrence Steinman
Keyword(s):  
Multiple Sclerosis ◽  
Immune Response ◽  
Clinical Trials ◽  
Immune Responses ◽  
Large Scale ◽  
Adaptive Immune Response ◽  
Antibody Responses ◽  
Myelin Proteins ◽  
Adaptive Immune ◽  
Key Drivers

ABSTRACT:The adaptive immune response in multiple sclerosis is complex. We have devised large scale arrays to measure the antibody response to myelin proteins and lipids. Despite the widespread immune responses to myelin, we have devised an inverse vaccine aimed at turning off key drivers of this diverse response. Clinical trials in patients with multiple sclerosis show that it is possible to constrain antibody responses to myelin on a large scale with this approach.

scholarly journals Insights into Innate Immune Response Against SARS-CoV-2 Infection

2021 ◽  
Vol 29 (3) ◽  
pp. 255-269
Author(s):  
Adina Huțanu ◽  
Anca Meda Georgescu ◽  
Akos Vince Andrejkovits ◽  
William Au ◽  
Minodora Dobreanu
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Innate Immune Response ◽  
Innate Immune System ◽  
Time Course ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Interferon Response ◽  
Humoral Factors ◽  
Key Steps

Abstract The innate immune system is mandatory for the activation of antiviral host defense and eradication of the infection. In this regard, dendritic cells, natural killer cells, macrophages, neutrophils representing the cellular component, and cytokines, interferons, complement or Toll-Like Receptors, representing the mediators of unspecific response act together for both activation of the adaptive immune response and viral clearance. Of great importance is the proper functioning of the innate immune response from the very beginning. For instance, in the early stages of viral infection, the defective interferon response leads to uncontrolled viral replication and pathogen evasion, while hypersecretion during the later stages of infection generates hyperinflammation. This cascade activation of systemic inflammation culminates with cytokine storm syndrome and hypercoagulability state, due to a close interconnection between them. Thus an unbalanced reaction, either under- or over- stimulation of the innate immune system will lead to an uncoordinated response and unfavorable disease outcomes. Since both cellular and humoral factors are involved in the time-course of the innate immune response, in this review we aimed to address their gradual involvement in the antiviral response with emphasis on key steps in SARS-CoV-2 infection.

scholarly journals Current Progress in the Development of Zika Virus Vaccines

Vaccines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1004
Author(s):  
Kehui Zhou ◽  
Chaoqun Li ◽  
Wen Shi ◽  
Xiaodan Hu ◽  
Kutty Selva Nandakumar ◽  
...  
Keyword(s):  
Zika Virus ◽  
Large Scale ◽  
Vaccine Development ◽  
Clinical Symptoms ◽  
Effective Vaccine ◽  
Zikv Infection ◽  
Teratogenic Effects ◽  
Subunit Vaccines ◽  
Live Attenuated Vaccines ◽  
Inactivated Vaccines

Zika virus (ZIKV) is an arbovirus first discovered in the Americas. ZIKV infection is insidious based on its mild clinical symptoms observed after infection. In Brazil, after 2015, ZIKV infection broke out on a large scale, and many infected pregnant women gave birth to babies with microcephaly. The teratogenic effects of the virus on the fetus and its effects on nerves and the immune system have attracted great attention. Currently, no specific prophylactics or therapeutics are clinically available to treat ZIKV infection. Development of a safe and effective vaccine is essential to prevent the rise of any potential pandemic. In this review, we summarize the latest research on Zika vaccine development based on different strategies, including DNA vaccines, subunit vaccines, live-attenuated vaccines, virus-vector-based vaccines, inactivated vaccines, virus-like particles (VLPs), mRNA-based vaccines, and others. We anticipate that this review will facilitate further progress toward the development of effective and safe vaccines against ZIKV infection.

scholarly journals Defective ORF8 dimerization in delta variant of SARS CoV2 leads to abrogation of ORF8 MHC-I interaction and overcome suppression of adaptive immune response

2021 ◽  
Author(s):  
Armi Chaudhari ◽  
Dr. Indira Singh ◽  
Dr. Madhvi Joshi ◽  
Dr. AMRUTLAL PATEL ◽  
Proff. Chaitanya Joshi
Keyword(s):  
Amino Acids ◽  
Immune Response ◽  
Adaptive Immune Response ◽  
Host Immune Response ◽  
Structural Instability ◽  
Salt Bridges ◽  
Wild Type ◽  
Mhc I ◽  
Second Wave ◽  
Short Timeframe

In India, the breakthrough infections during second wave of COVID-19 pandemic was due to SARS-COV-2 delta variant (B.1.617.2). It was reported that majority of the infections were caused by the delta variant and only 9.8% percent cases required hospitalization whereas, only 0.4% fatality was observed. Sudden dropdown in COVID-19 infections was observed within a short timeframe, suggesting better host adaptation with evolved delta variant. Down regulation of host immune response against SARS-CoV-2 by ORF8 induced MHC-I degradation has been reported earlier. The Delta variant carried mutations (deletion) at Asp119 and Phe120 amino acids which are critical for ORF8 dimerization. The deletions of amino acids Asp119 and Phe120 in ORF8 of delta variant results in structural instability of ORF8 dimer caused by disruption of hydrogen bonding and salt bridges as revealed by structural analysis and MD simulation studies of ORF8 dimer. Further, flexible docking of wild type and mutant ORF8 dimer revealed reduced interaction of mutant ORF8 dimer with MHC-I as compared to wild type ORF8 dimer with MHC-1, thus implicating its possible role in MHC-I expression and host immune response against SARS-CoV-2. We thus propose that mutant ORF8 may not hindering the MHC-I expression thereby resulting in better immune response against SARS-CoV-2 delta variant, which partly explains the sudden drop of SARS-CoV-2 infection rate in the second wave of SARS-CoV-2 predominated by delta variant in India

scholarly journals SARS-CoV-2: From Structure to Pathology, Host Immune Response and Therapeutic Management

2020 ◽  
Vol 8 (10) ◽  
pp. 1468
Author(s):  
Grigore Mihaescu ◽  
Mariana Carmen Chifiriuc ◽  
Ciprian Iliescu ◽  
Corneliu Ovidiu Vrancianu ◽  
Lia-Mara Ditu ◽  
...  
Keyword(s):  
Immune Response ◽  
Molecular Mechanisms ◽  
Prolonged Exposure ◽  
Vaccine Development ◽  
Host Immune Response ◽  
Physical Factors ◽  
Respiratory Pathogens ◽  
Inflammatory Conditions ◽  
Multiplication Cycle ◽  
Wide Range

Coronaviruses are large, enveloped viruses with a single-stranded RNA genome, infecting both humans and a wide range of wild and domestic animals. SARS-CoV-2, the agent of the COVID-19 pandemic, has 80% sequence homology with SARS-CoV-1 and 96–98% homology with coronaviruses isolated from bats. The spread of infection is favored by prolonged exposure to high densities of aerosols indoors. Current studies have shown that SARS-CoV-2 is much more stable than other coronaviruses and viral respiratory pathogens. The severe forms of infection are associated with several risk factors, including advanced age, metabolic syndrome, diabetes, obesity, chronic inflammatory or autoimmune disease, and other preexisting infectious diseases, all having in common the pre-existence of a pro-inflammatory condition. Consequently, it is essential to understand the relationship between the inflammatory process and the specific immune response in SARS-CoV-2 infection. In this review, we present a general characterization of the SARS-CoV-2 virus (origin, sensitivity to chemical and physical factors, multiplication cycle, genetic variability), the molecular mechanisms of COVID-19 pathology, the host immune response and discuss how the inflammatory conditions associated with different diseases could increase the risk of COVID-19. Last, but not least, we briefly review the SARS-CoV-2 diagnostics, pharmacology, and future approaches toward vaccine development.

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