Virus immune response animation

B cells produce antibodies that help to control microbial invasion in a variety of ways, as described in this interactive. With your new knowledge about antibodies, you are ready to see an example of the B cell response in action. In this interactive, the reaction of B cells to an invading pathogen is shown, including how the antibody response arises and how it is able to control the infection. While the response to a bacterial protein is shown, the steps necessary to act against viruses such as the coronavirus that causes COVID are very similar.

Antibody responses are the main way in which vaccines protect us from infection by a variety of viruses, and the absence of protective antibodies contributes to the rapid spread of new viruses in previously unexposed and unvaccinated populations. The antibodies produced by B cells form part of the adaptive immune response and can recognize almost any molecule that might invade the body.

In addition, there is a second branch to the adaptive immune system called cellular immunity. T cells form the basis of cellular immunity and can very specifically kill cells that have been infected by viruses.

This video compares the two branches of the adaptive immune response, with a particular emphasis on the antiviral effects of T cells. T cells form the second branch of the adaptive immune response. Unlike B cells, the receptors on T cells are only able to recognize protein fragments displayed on specific cell surface molecules. In this interactive, you will learn about the different types of T cells, including cytotoxic T cells that kill infected cells and helper T cells that increase the activation of other immune cells.

Full Screen T Cell Responses to Viral Infections While the innate immune and B cell responses are effective against a wide variety of pathogens, T cells can respond very specifically to intracellular pathogens, such as viruses. In this interactive, you will walk through an example of a T cell response to a viral invasion, as would occur in the case of COVID In a recent reverse genetic investigation, it was found that after interfering with NS1, the phosphorylation level of PKR dramatically increased, which was attenuated by forced expression of vault RNAs Importantly, NS1 is not only involved in host innate immunity, but also affects adaptive immunity via modulating the maturation and the capacity of DCs to induce T cell responses Investigation on the interaction between the virus and host by systematic biology analysis has revealed that PB2 protein, a member of the viral polymerase complex, also plays roles in IFN antagonism Recently, viral M2 protein has been found to interfere with the host autophagy , These studies have suggested that viral M2 may inhibit the activation of TLR pathway and the generation of IFNs via blocking the host autophagy.

It is well known that host immune response to IAV infection comprises multiple intricate processes that coordinate together to play significant roles in the protection of host. Given the high mutation rate of IAVs, it is necessary to have effective vaccination strategies that can induce robust production of specific antibodies and long-lived T cell response to defend against the viral infection.

Since host innate immunity is also critical for anti-IAV infection, further efforts are needed to utilize the current knowledge and technology to enhance the host innate immunity for control of the disease.

While our understanding of the IAV-host interaction has increased profoundly, extensive studies are required to better understand the dynamics of host immune system upon detection of the evolved IAVs.

Bridging these gaps will pave the way not only for designing better vaccines and effective vaccination strategies but also for developing novel antiviral agents. MM and SH revised the manuscript. J-LC organized and provided the frame for the manuscript and critically revised the manuscript.

All authors read and approved the final manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

The reviewer HZ and handling editor declared their shared affiliation. National Center for Biotechnology Information , U. Front Immunol. Published online Mar 5. Author information Article notes Copyright and License information Disclaimer. Specialty section: This article was submitted to Microbial Immunology, a section of the journal Frontiers in Immunology.

Received Jul 28; Accepted Feb 5. The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

This article has been cited by other articles in PMC. Abstract Influenza A viruses IAVs are contagious pathogens responsible for severe respiratory infection in humans and animals worldwide.

Keywords: influenza A virus, immune response, innate immunity, adaptive immunity, immune evasion. Introduction Influenza viruses belong to the Orthomyxoviridae family, which is characterized by a segmented, negative sense, and single-stranded RNA ssRNA genome 1. Activation of Innate Immune Signaling upon Intracellular Detection of IAV Infection The innate immune response is the first line of defense against viral infection which is rapid in response, but nonspecific. Open in a separate window.

Figure 1. Role of s-IgA Antibody in Defense against the IAV Infection Secretory IgA is the primary isotype detected at the mucosal surface , which contributes to mucosal protection through its distinct ability to remove an agent before it traverses the mucosal barrier and infects the cell Conclusion It is well known that host immune response to IAV infection comprises multiple intricate processes that coordinate together to play significant roles in the protection of host.

Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Footnotes Funding. References 1. Intracellular colocalization of influenza viral RNA and Rab11A is dependent upon microtubule filaments.

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