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Immune Response to Infectious Disease PowerPoint Presentation

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Description : Check out this medical presentation on Influenza (Flu), which is titled "Immune Response to Infectious Disease", to know about the immune response to infectious disease.

Tags : Influenza, Flu, Immune Response, Infectious Disease, Immunity

Published on : Jul 12, 2021 | Views : 1793 | Downloads : 5

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IMMUNE RESPONSE TO INFECTIOUS DISEASE By: Erin Anthony Yasmin Deliz Jasminia Nuesa
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INTRODUCTION Despite innate and adaptive immune responses to pathogens, infectious diseases which have plagued human populations throughout history still cause millions of deaths per year. There are 4 main types of pathogens that cause infectious disease 1. Viruses 2. Bacteria 3. Protozoa 4. Helminths
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VIRAL INFECTIONS One of the 4 main pathogens responsible for infectious diseases Responsible for smallpox, the common cold, chickenpox, influenza, shingles, herpes, polio, rabies, Ebola, hanta fever, and AIDS. Several specific immune effector & nonspecific defense mechanisms Viruses act to subvert one or more of these mechanisms to prolong their survival
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VIRAL INFECTIONS Viruses: Structure & Function Viruses depend on host cells for reproduction Outside of host cells, the viruses remain metabolically inert They exist as a protein coat or capsid, sometimes enclosed within a membrane The capsid encloses either DNA or RNA which codes for the virus elements
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VIRAL INFECTIONS Viruses: Structure & Function (cont.) In contact with a cell, the virus, with help from surface molecules, will inject it’s genetic material into the cell Thus taking over the cell’s functions The infected cell produces more viral proteins and genetic material rather than it’s usual products In the cell, the virus has two phases: 1. The lysogenic phase 2. The lytic phase
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VIRAL INFECTIONS
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VIRAL INFECTIONS Innate Immune Response - 2 primary events: 1. Induction of Type I Interferons 2. Activation of NK cells
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VIRAL INFECTIONS Induction of Type I Interferons: The double-stranded RNA (dsRNA) of the virus induces the expression of the interferons by the infected cell. The bound IFN’s will activate the JAK/STAT pathway responsible for the synthesis of several genes One encodes 2-5(A) synthetase an enzyme that activates ribonuclease (RNAse L)
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VIRAL INFECTIONS IFN’s and NK Cells In addition, IFN-α & IFN-β binding induces a specific protein kinase called RNA-dependent protein kinase (PKR) The binding of IFN-α & IFN-β to NK cells induces lytic activity Effective in killing virally infected cells Enhanced by IL-12
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VIRAL INFECTIONS
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VIRAL INFECTIONS Viral Neutralization by Humoral Antibody What is crucial to the preventing of the spread of the virus during acute infection and in protecting against reinfection? ANTIBODIES If antibody is produced to the viral receptor, it can block infection altogether by preventing viral binding to the host cells i.e. Secretory IgA in mucous secretions Viral Neutralization by antibody sometimes occurs after viral attachment Some may block viral penetration by binding to epitopes necessary to mediate fusion of the viral envelope with the plasma membrane Some cause the lysis of the enveloped virions Some agglutinate viral particles and function as an opsonizing agent
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VIRAL INFECTIONS Cell-Mediated Antiviral Mechanisms Antibodies, although crucial in containing the spread of the virus, are not able to eliminate the virus once infection has occurred Once infection occurs, cell-mediated immune mechanisms become the most important 2 main components of cell-mediated antiviral defense 1. CD8+ Tc cells 2. CD4+ Th1 cells (CD4+ Tc cells)
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VIRAL INFECTIONS Cell-Mediated Antiviral Mechanisms (Cont.) Activated Th1 cells produce several cytokines IL-2 Acts indirectly by assisting in the recuitment of CTL precursors Activates NK cells IFN-γ Directly induces an antiviral state in cells Activates NK cells TNF CTL activity Arises within 3-4 days after infections Peaks by 7-10 days, and then declines Have viral specificity Eliminites specific virus-infected cells, thus getting rid of potential new sources of new virus
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VIRAL INFECTIONS Viral Invasion of Host-Defense Mechanisms Viruses encode proteins that interfere at various levels with specific or nonspecific host defenses Some develop strategies to avade the action of IFN-α & IFN-β Some inhibit the antigen presentation by infected hosts by preventing antigen delivery to class I MHCs Some reduce levels of class II MHCs on cell surface Others evade complement-mediated destruction Some cause generalized immunosuppression-direct viral infection of lymphocytes or macrophages Some constantly change their antigens i.e. Influenza
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VIRAL INFECTIONS Properties of the Influenza Virus Virions are roughly spherical or ovoid in shape with an ave. diameter of 90-100nm Virions are surrounded by an outer envelope 2 proteins are inserted into this envelope 1. Hemagglutinin (HA) 2. Neuraminidase (NA) Inside the envelope: Matrix protein surrounds the nucleocapsid Consists of 8 different strands of ssRNA associated with protein and RNA polymerase
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VIRAL INFECTIONS Influenza 3 major types– A, B, &C Distinguished by differences in their nucleoprotein and matrix proteins Distinguishing feature of influenza virus is its variability Two different mechanisms for variation in HA & NA 1. Antigenic Drift 2. Antigenic Shift
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VIRAL INFECTIONS Influenza (Flu) Symptoms: Fever Muscle aches and pain Headache Fatigue Dry cough Sore throat Runny nose What makes this different from a cold?
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VIRAL INFECTIONS Host Response to Influenza Infection Humoral Antibody specific for the HA molecule is produced during infection Serum antibodies antibodies imporant for resistance to reinfection by the same strain, but not required for recovery In addition, CTLs also play a role
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VIRAL INFECTIONS Epstein-Barr (Infectious Mono) Herpes virus family Life-long dormant infection in some cells Symptoms: Fever Sore Throat Swollen Lymph glands Swollen liver/spleen *Age Group*
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