Host Immune Evasion
Host Immune Evasion - Related Videos
08:32
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Cited by 2 •
2014
We describe a protocol to measure the antiviral cytokine production in mice infected with a model herpesvirus, murine gamma herpesvirus 68 (γHV68) that is closely-related to human Kaposi’s sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). Utilizing genetically modified mouse strains and mouse embryonic fibroblasts (MEFs), we assessed the antiviral cytokine production both in vivo and ex vivo. “Reconstituting” the expression of innate immune components in knockout embryonic...
02:46
Intranasal Murine Herpesvirus Infection in Mice to Assess Host Immune Responses
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2026
Source: Zhang, J., et al. P. Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production. J. Vis. Exp. (2014)This video demonstrates intranasal delivery of murine herpesvirus in mice to induce a lung-specific immune response. Lung tissue is subsequently processed to obtain cytokine-containing supernatants for downstream assessment of host immune responses.
12:27
The Utilization of Oropharyngeal Intratracheal PAMP Administration and Bronchoalveolar Lavage to Evaluate the Host Immune Response in Mice
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Cited by 15 •
2014
The host immune response to pathogen infection is a tightly regulated process. Utilizing a lipopolysaccharide lung exposure model in mice, it is possible to conduct high resolution evaluations of the complex mechanisms associated with disease pathogenesis.
09:07
Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses
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Cited by 16 •
2017
Systemic and localized zebrafish infection models for human influenza A virus are demonstrated. Using a systemic infection model, zebrafish can be used to screen antiviral drugs. Using a localized infection model, zebrafish can be used to characterize host immune cell responses.
02:18
Live Imaging of Host-Pathogen Interactions in Zebrafish Embryos Infected with Mycobacterium abscessus
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2026
Source: Bernut, A., et al. Deciphering and Imaging Pathogenesis and Cording of Mycobacterium abscessus in Zebrafish Embryos. J. Vis. Exp. (2015)This video demonstrates a protocol that uses transgenic zebrafish embryos expressing fluorescent macrophages and infected with fluorescent Mycobacterium abscessus rough strain to visualize host-pathogen interactions. It reveals how extracellular cording enables immune evasion, promoting bacterial survival and host cell damage.
FAQs
Altering surface antigens changes the molecular features that immune defenses use to identify a target. When those features no longer match previously recognized patterns, immune recognition can become less effective, allowing the pathogen or abnormal cell to persist. In research, this mechanism helps explain incomplete immune control and why recognition-focused interventions may lose effectiveness.
Once a pathogen remains within host cells, it is less directly exposed to immune defenses operating outside those cells. This location can also intersect with mechanisms that block antigen presentation, reducing the display of pathogen-derived information to immune cells. Studying these linked strategies helps explain persistence and provides context for approaches intended to restore effective immune recognition.
Interference with complement or cytokine signaling disrupts communication and effector functions that coordinate host defense. Complement contributes to immune attack, while cytokine signals regulate activation and communication among immune cells. Blocking either pathway can reduce the strength or coordination of the response, making it harder for the host to eliminate a persistent pathogen or abnormal cell.
Examining these strategies can connect specific disruptions, such as blocked antigen presentation or reduced immune-cell activation, with the persistence of infection. This research helps explain why some infections become chronic rather than being cleared quickly. It also identifies immune processes that may need reinforcement or restoration when developing antimicrobial therapies or other interventions.
In tumors, reduced immune surveillance can allow abnormal cells to remain undetected or insufficiently controlled. Research therefore examines how altered surface antigens, impaired antigen presentation, and reduced immune-cell activation contribute to tumor persistence. These findings provide biological context for immunotherapies designed to improve recognition or strengthen effective immune responses against abnormal cells.
Mapping immune-evasion strategies can guide vaccine design by highlighting the immune features that must be recognized despite antigen alteration or signaling interference. The same knowledge supports antimicrobial therapies and immunotherapies, as well as strategies intended to restore effective immune recognition. Mechanistic findings therefore connect pathogen or tumor persistence with possible ways to improve host control.