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147 Cards in this Set
- Front
- Back
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The structure of a virus consists of ____, _____, and _________
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Envelope
Matrix Protein Capsid |
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7 Steps in Virus Infection
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1. Virus binds to specific receptor
2. Penetrates membrane (endocytosis) 3. Nucleic acid of virus released from virus coat 4. Virus NA detects synthesis of viral proteins 5. Virus NA replicates 6. Virus particles assemble from NA & virus protein 7. Virus release from cells via budding (enveloped form from cell membrane) or lysis (no envelope) |
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When a virus is release from cells via budding the __1___ is formed from the cell membrane, while when a cell lysis no __1___ is formed.
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1. envelope
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What cytokines are made by infected cells in cell mediated host defense?
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IFN alpha, beta, gamma
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In cell mediated defense against viral infection, IFN alpha and beta induce synthesis of _______.
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DAI - double-stranded RNA activated inhibitor of translation
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In cell mediated defense against bacteria, DAI binds to ________ and is activated, inhibiting ALL _________ in the infected.
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-double-stranded RNA
-protein synthesis |
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In cell mediated host defense, interferon gamma directly inhibits ____ ____ and stimulates ________ activity, activating NK cells.
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inhibits viral replication
MHC I activity |
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Interferon gamma inhibits viral replication by:
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-binding to specific receptors (STAT signaling - antiviral protein synthesis)
-Inhibit viral polymerase -Activating ribonucleases to degrade viral DNA -Prevent capsid assembly |
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How do viruses evade Natural Killer cells?
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downregulate MHC Class I
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What cell mediated host defense controls early infection before primary T cell response (hint: apoptosis)
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Natural Killer Cells
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What are the 3 cell mediated defenses listed for protection against virus infection?
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-Interferon (a, b, g)
-Natural Killer Cells -T Cells |
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How do Cell mediated T Cells defend against a viral infection?
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-Pore forming peptides
-Apoptosis of activated cells -Produce IFN gamma -STimulate B cells to produce IgM, Ab class switching --> greater affinity |
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How does the humoral response prevent virus and reinfection?
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-block virus binding tocellular receptors
-prevent virus entry - prevent uncoating of virions (prevent release of NA) -prevent viral release from cells -mediate cell and virus destruction (ADCC, NK cell activation by Fc receptors) |
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How does complement pretect host from viral infection?
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-damage to viral envelope
-block virus receptor -direct virolysis -opsonization of coated virus ---> phagocytosis -lyse infected cells |
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Difference between HIV 1 and HIV 2?
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HIV 1 - Pandemic, quicker progression to AIDS, MNOP strains
HIV 2 - Slow disease progression, West Africa |
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outer envelope of lipid bilayer of HIV is made up which embedded proteins?
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gp120 cap and gp41 stem
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HIV Life cycle Initiation:
gp120 of the virus binds to ___1___ on cell surface. The virus twists, exposing the ___2___ or ______. __3__ attaches to the chemokine, fusing the virus to the cell. Upon fusion the virus releases its _______ into the cell, containing its RNA, proteins, and enzymes |
1. CD4+ molecules. (CD4+ T cells, monocytes, macrophages)
2. CXCR4 or CCR5 chemokines 3.gp41 4.capsid |
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Reverse transcription of HIV viral RNA into ___1____ occurs in the __2___ of the cell. HIV __1__ migrates to cell nucleus and is spliced into host DNA by __3___.
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1. DNA
2. cytoplasm 3. HIV integrase (provirus) |
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The transcription of HIV viral DNA into viral mRNA may be initiated by __1___ or __2__. The protein that accelerates the process is ____3____
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1. cytokines (TNFa, IL-6)
2. other infections (eg. M. tb) 3. viral tat gene |
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After HIV mRNA translation, HIV proteins proteins aggregate and leave the cell through __1___ (acquiring ___2___) OR can form a ____3___
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1. budding
2. envelope 3. multinucleate giant cell (cell to cell transmission) |
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In the primary phase of HIV infection APCs (dentritic cells) infected and transport virus to __1___. Large numbers of __2___ infected and killed. Increase in __3_ cells.
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1. lymph nodes
2. CD4+ T cells 3. CD8+ Killer T |
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HIV infection of the lymphoid tissue:
Follicular dendritic cells present virus to __1__, initiatiating a humoral response. __2____ become attracted to the infected cells coated with antibody, and become infected themselves |
1. B Cells
2. CD4+ |
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Within the lymphoid tissue, HIV infects monocytes and macrophages, which release the cytokines, _1___ and ____, which activate ____2___ cells. ___2__ lose the capacity to make IL-2.
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1. TNFa and IL-6
2. CD4+ T |
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CD4+ cells infected with HIV lose the ability to to make _____ (which enhances growth and stimulate other T cells to resist invaders)
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IL-2 ---- decrease receptors as well
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How are CD8+ T cells important durign acute infection and clinically latent stages of HIV?
Biggest issue?? |
-attack and kill infected cells producing virus
-secrete soluble factors that suppress HIV replications -occupy receptors necessary for entry of HIV into target cells -Kill infected T cells (CD4 Helper T)....which they are dependent on |
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HIV Evasion Strategies
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-Reduce competitive bindfing for CCR chemokine by shifting from M-tropic (CCR5) to T-tropic (CXCR4) during late disease
-Virus not exposed to antibody in follicular dendritic cells -Deceases MHC I expression -Latent reservoir in non-activated CD4 -CTL clonal exhaustion -Reservoir in bone marrow multi-potent porgenitor cells -HIV genetic variation |
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People who lack _____ are resistant to HIV infect
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CCR5
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Forms of HIV genetic variation to to evade immune response
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-reverse transcriptase copying errors
-recombination between virus strains -escape antibody or killer T cells -Drug resistance |
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How does HIV lead to immune system loss?
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-direct cell killing (budding)
-syncytium (fusion of cells) formation -apoptosis -superantigen -anergy (HIV turns off cells) damage to precursor cells (bone marrow/thymus) |
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HIV - Testing methods
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-IgG Elisa - screening
-Western Blot confirmatory -CD4, CD8 in blood -viral load virus isolation |
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Hepatitis A
Source of Virus Route of Transmission Chronic Infection Prevention |
-Feces
-Fecal Oral -No -Immunization |
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Hepatitis B
Source of Virus Route of Transmission Chronic Infection Prevention |
-Body/fluids
-precutaneous, premucosal -Yes -Immunization |
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Hepatitis C
Source of Virus Route of Transmission Chronic Infection Prevention |
-Body/fluids
-precutaneous, premucosal -Yes -Blood donor screen, risk modification |
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Hepatitis D
Source of Virus Route of Transmission Chronic Infection Prevention |
-Blood/fluids
-precutaenous, premucosal -Yes -risk behavior modification |
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Hepatitis E
Source of Virus Route of Transmission Chronic Infection Prevention |
-Feces
-fecal-oral -no -ensure safe drinking water |
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-ds DNA hepadnavirus
-transmitted via blood/body fluids -Outer envelope of surface proteins and inner core with protein coat -Core releases DNA and polymerase into hepatocyte nucleus -long incubation |
Hepatitis B
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Hepatitis B _______ protein release DNA and polymerase into ______ nucleus, which produce the virus' proteins. NOT REVERSE TRANSCRIPTASE
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Core (HBc)
hepatocytes |
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During Hep B infection _1__ & _____ are the first things detected in the blood stream. __2__ is not detectable in lab assays. __3__ appears only after viral replication. ___4__ detectable when virus is actively reproducing.
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1. DNA and DNA polymerase
2. HBcAg 3. HBsAg 4. HBeAg |
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The first detectable antibody of Hepatitis B is the ___1___, which indicates an infection rather than an vaccination. _2___ antibody is a marker of immunity. This Ab (_3___) appears after HBeAg no longer detected
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1. HBcAb
2. HBsAb 3. HBeAb |
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What is the difference between Acute and Chronic Hepatitis B virus?
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The Acute virus has Antibody to HBs antigen (HBsAb), sign of recovery. Acute also has HBeAb.. Chronic carrier has persistent of HBsAg and HBeAg
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The hepatitis B vaccine induces immunity to ______ antigen
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surface antigen (HBsAg)
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-ssRNA Delta Virus
-has Hep B surface antigen (HBsAg) -percutaneous & permucosal transmission --Coinfection/Superinfection with Hep B |
Hepatitis D
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During a Hep B-D coinfection, what antibody is required for the suppression of the disease that is not present in chronic Superinfection?
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Hepatitis B surface antibody (HBsAb)---necessary for suprresion of HBsAg and Hep D RNA
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Preventative methods for HBV-HDV coinfection? Superinfection?
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- Hep B Vaccine for coinfection
- risk behavior modification for super |
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-ssRNA flavivirus
-percutaneous and permucosal transmission -decreasing incidence, but continued prevalence (until death) -most people asymptomatic chronic carriers -cirrhosis, portal hypertension, hepatic failure -most frequent cause of liver transplant -Lots of gentoypes |
Hepatitis C
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Genetic heterogeneity of the HCV isolates within an individiual
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HCV quasispecies
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Different percutaenous methods of methods for transmission of HCV?
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-Injection drug use
-Clotting factors -transfusion/transplant -Occupational |
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Why do those with acute HCV infection progress to Chronic infection?
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-Antibody to HCV does not neutral the HCV RNA or ALT
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Are immunoglobulin and antivirals recommended for post exposure prophylaxis of Hep C?
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No - antibodies did not work
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Testing for HCV
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-EIA Screening
-RIBA confirmation (immunoblot similar to Western blot) |
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Hepatitis C treatment recommendations
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-Antiviral therapy (mono and combo)
-avoid alcohol -avoid behavioral risk -Hep A& B vaccination -Liver transplant |
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Flavirus that is a relative of Hepatitis C
-Replicates in peripheral blood monoscytes -Frequently coexists with HCV & HIV infections and MAY inhibit HIV replication |
Hepatitis G
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-ssRNA picornavirus
-transmitted by close personal contact or contaminated food and water (fecal oral) -associated with community wide outbreaks -single serotype nationwide -acute and asymptomatic --> NO CHRONIC -Protective antibodies with lifelong immunity |
Hepatitis A
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Hepatitis A Prevention
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-Vaccine
-Hygiene/Sanitation -Immune Globulin |
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_____ serve as a reservoir for Hep A virus
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children
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Is a risk factor identified for most community wide outbreaks of Hepatitis A?
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No
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-Hepatitis out break associated with fecally contaminated water (not common in the US)
-minimal person-to-person transmission -zoonotic disease found in swine -pig handlers and veterinarians are at greatest risk -similar serological course to Hep A |
Hepatitis E
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Hep E has 5 genotypes
Type 1 & 2 in ? Type 3 & 4? Type 5 |
1 & 2 - humans
3 & 4 - humans and pigs 5 avian |
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What is xenotransplantation?
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Pig transplants. The use of pig parts, such as heart valves, in human transplants
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Prevention and control for travelers to HEV-Endemic areas?
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-avoid drinking water and uncooked food or vegetables
-Immune globulin from Western Donors not helpful since disease not exist here |
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Anatomy of the Influenza Virus
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-Lipid envelope from cell membrane
-Hemagglutinin & neuraminadase -8 single stranded RNA segments |
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_______ facilitates the mobility of influenza virions by cleaving viral _____ during entry and release from cells
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-Neuraminiadase (NA)
-Hemagglutinin |
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The inititial step in influenza infection (receptor binding) is mediated by the _________ ______
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Hemagluttinin glycoprotein
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Pathogenicity of influenza virus is determined by the presence of what amino acids at the cleavage site of Hemagluttinin?
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lysin and arginine
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Influenza NS1 protein is synthesized in ___1____ cells. NS1 Binds to and inhibits cellular protein synthesis and __2___ production that modify 3' ends of __3____. At the carboxyl end of NS1 in H5N1, __4__ proteins are important in normal cell signaling and maintenance of human cellular structure and organization.
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1. infected
2. interferon b 3. mRNA 4. PDZ proteins |
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Virulent flu A strains _____ protein has glu-ser-glu-val @ its carboxyl end that mediates binding human PDZ . Low virulent influenza strains do not have this AA sequence and do not bind PDZ
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NS1
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Influenza antibody is made to the ___1__ proteins.
Antibody to _2___ is neutralizing antibody. Antibody to __3___ is infection permissive but disease suppressive |
1. surface antigen proteins
2. Hemagluttinin (prevents infection) 3. Neuraminadase |
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Poitn mutations that result in variation in protein composition leading to changes in antigenic structure and loss or prior antibody match
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Antigenic Drift
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Recombination of different strain genomes that creates new types of Hemagglutinin or Neuraminadase in virus with human transmissivity genes
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Antigenic Shift
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How does Human pandemic strains of influence A virus appear?
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-Reassortment of genes within a permissive host (pig)
-transmission of an infectious strain from one species to another -reappearance of a strain which had been hidden and unchanged for some time |
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Influenza virus binding is mediated by the ______ binding to ____ on cell surface
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hemmaglutinin glygoproteins
sialic acid |
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Hemagglutinin membrane glycoprotein- sialic aicd binding linkages
1 avian 2. human 3. swine 4. human respiratory tracts (a. nose.throat, b. alveoli) |
1. alpha 2,3
2. alpha 2,6 3. alpha 2,3 and a 2,6 4. a. a 2,6 b. a 2,3 |
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Beyond __1___-_______ linkage, influenza receptor binding is determined by the ___2__ of the glycan receptor and _3____ of the sugar chain. Bird receptors are 4___ and ___, while humans are __5_ and ___.
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1. hemagglutinin-sialic acid
2. topology 3. length 4. coned and short 5. umbrella and long |
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Protein that prevent the spread of influenza virus in lungs (possibly others
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IFITM3 (interferon inducible transmembrane protein)
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Influenza assays include
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Rapid Antigen Tests (EIA)
-RT-PCR -virus isolation -retrospective (HAI & ELISA) |
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ds DNA viruses
-replicate and assemble in nucleus -glycoprotein envelope -isolated from many animal species -modulate host immune response through latent infections and secrete "version" of cellular cytokine receptors |
Herpes virus
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Alphaherpes includes what viruses
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HSV1, HSV2: herpes, cold sores, genital ulcers
Varicella Zoster virus: shingles, chickenpox |
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In Alphaherpes, degradation of host mRNA and shutoff of host protein synthesis occurs in all cells but ________.
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neural cells
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Neurons are resistant to _______, which causes a _______ infection.
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Virion host shutoff protein
latent infection |
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How do latent infections in the sensory neurons avoid the immune system?
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-travel along axons
cell to cell transmission -latency associated transcripts (LATs) promote neural survival by inhibiting apoptosis |
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Alphaherpes latency can be reactivated by:
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physical
psychological stimulus immunosuppression |
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How is a baby infected with alpha herpes?
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-during birth
-soon after birth from contact with oral and skin lesions |
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Lab diagnosis of Alpha herpes includes:
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-PCR, culture, and IFA of lesions scrapings
-Serology (4 fold rise in titer) |
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Beta herpes viruses include
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-Cytomegalo (CMV) (HHV-5)
-HHV-6 -HHV-7 |
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-asymptomatic, universal, herpes virus that can be transmitted by blood or organ donation (urine, saliva, tears, semen, breast milk as well).
-Produces a protein that binds MHC I and preventing it from being expressed on infected cell surface |
Betaherpes Cytomegalovirus
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Reactivation of Cytomegalovirus betaherpes most common in those who are _________. They may experience frequent severe infections including:
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T cell defects (immunosuppresed)
-pneumoniitis, GI disease, retinitis |
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Herpes virus whose primary infection childhood causes 6th disease, roseola infantum
-In adults primary infection leads mono or hepatitis -80% adults carry Ab |
Betaherpes HHV-6
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Little known herpes disease that causes fever, rash, seizures,and may be a co-factor in HHV-6 syndromes
-98% adult have positive antibody |
Beta herpes HHV-7
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Gamma Herpes virus includes:
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Epstein-Barr Virus (HHV-4)
HHV-8 |
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Gamma herpes Epstein-Barr virus infection leads to____1___ activation and proliferation. Once infected a person becomes a ____2_____.
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1. polyclonal B cell activation and proliferation
2. lifelong carrier |
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The primary Epstein-Barr virus infection that leads to fever, lymphadenopathy, splenogomy and jaundice.
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Infectious Mononucleosis
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Gamme herpes EBV that is endemic to in parts of Africa and Papua New Guinea
-malaria infection is a cofactor -Patients with this disease have high titers of Ab against various EBV antigens -Translocation between long arm of chromosomes |
Burkitt's lymphoma
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-a malignant tumor of squamos epithelium of the nasopharynx caused by a gamma herpes EBV
-contains multiple copies of EBV genome and EBV EBNA-antigen within cells -antibodies against various EBV antigens |
Nasopharyngeal Carcinoma
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Gamma herpes EBV In immunocompromised patients results in
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-Latent virus reactivation
-Ducan X-linked lymphoproliferative syndrome |
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Immunocompromised EBV patients receiving a transplant develop ______1___, while AIDS patients develop ___2___ ____ and ___3____.
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-Lymphoma
-oral leukoplakia -Non-Hodgkin's lymphoma |
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Males with a defective gene in the X chrmosome who lack T-cell produced signaling protein and is troublesome for those with EBV
-Hyperimmune response: cannot control B-cell proliferation leading to inflammatory response |
-Ducan X linked lymphoproliferative syndrome
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high risk groups with gamma herpes virus associated with Kaposi's sarcoma (AIDS), where viral proteins acts as immunomodulatory factors
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HHV-8
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-ss + sense RNA Virus
-3 strugctural protein in viral capsid with lipid bilayer (capsid, membrane, envelope) -receptor mediated endocytosis -includes Japanese encephalitis complex and Dengue |
Flavivirus
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After binding to the receptor, a flavivirus enters a cell via _______
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endocytosis
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Flaviviruses that replicates in capillary endothelium and in regional lymph nodes
-viremia circulates virus to muscle, connective tissue and to CNS |
-St Louis Encephalitis and West Nile
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Dengue virus vector
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Aedes aegypti
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time between when a mosquito feeds and acquires virus & when it re-feeds and transmits the virus
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Extrinsic incubation period
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time period between when a mosquito transmits a virus and when the person shows viremia
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Intrinsic incubation period
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Infection in an individual who has pre-existing antibody to a closely related antigen elicits both homotypic (to the current infecting strain) and heterotypic (to the original infecting strain) antibody development
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Original Antigen Sin
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In Dengue Hemorrhagic Fever, the antibody binds to virus from a second infecting strain and enhances bind to the Fc receptors on the cell surface which:
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-enhance virus uptake by macrophages
-INFLAMMATORY RESPONSE: hyperactivates the complement system, histamine, TNF, thromboplastin -cell lysis, vascular permeability, shock |
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T/F SLE, DEN, and WNV cross react in route screening assays
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True
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The neutralizing antibody in West Nile Virus is ....
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IgG
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In a clinical case between SLE, DEN, and WN what assays can be done to determine the disease?
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=Acute (day 6-10) and convalescent (14-21) serum compares
-specific IgM antibody confirmed by specific IgG antibody -specific virus IgM in CSF (cannot cross blood-brain barrier) -virus isolation/PCR |
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Flavivirus Clinical Specimens-Test flow chart:
1. If serum collected <5 days post onset ? 2. If serum collected between 5 and 9 days? 3. If serum colected >9 post onset? 4. How does one confirm a positive IgM or IgG? |
1. PCR and Virus isolation
2. IgG or IgM ELISA (negative inconclusive....positive needs confirmation) 3. IgG or IgM ELISA (negative confirmed...positive needs confirmation) 4. IgM in CSF, specific IgG, convalescent serum |
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Rheumatoid factor has non-specific reactions with the antigens, resulting in positive or negative tests to all antigens?
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positive
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Front line screening assay for West Nile Virus?
Issue with this test? |
IgM Mac ELISA
Found positive blood more than 1 yearout in 50% of cases |
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Why are secondary flavirviruses problematic in detection?
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No clear "winner"...all may be high in neutralization test
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Antibody controls infection (clears most but not all viremia), however ________ cells are required to clear virus from tissue (spleen).
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CD8+ T Cells
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In order to develop an effective vaccine immunity to the agent must occur in _____ and we must understand how that immunity is produced
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nature
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Vaccination is responsible for (4)
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Disease prevention
Reduce Disease severity Outbreak prevention for contagious disease Herd immunity |
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Vaccinations induce production of ______ cells that will rapidly produce protective _____ or antigen specific _____ when the individual is exposed to the same infectious agent in nature
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memory cells
antibody T cells |
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protection generated by person's own immune system; results from infection or vaccination; may include cell mediated immune response
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Active Immunity
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protective factors (pre-formed antibodies) from one animal are transferred to another (natural maternal antibodes, immune globulin, antitoxin, humanized monoclonal Ab)
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Passive Immunity
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Problems with passive immunity:
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-Does not activate immune system (no T cells)
-No memory response (transient protection) -Serum sickness -Infectious agents/abs to recipient tissue -production and supply issues -Does not last |
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Serum sickness in passive immunity
-IgE binds to immune complexes in tissue ----> ___1___ and _____ -Igm & IgG to foreign species protein --->____2_ and _____ |
1. mast cell degranulation and system anaphylaxis
2. complement activation and type III hypersensitivity |
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The ability of antigen to bind to antibody (does not necessarily activate B cell to produce Ab)
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antigenicity
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ability of antigen to induce an immune response
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immunogenicity
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small antigenic epitopes that bind to antibodies but must be bound to a carrier molecule to induce antibody production
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haptens
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Fora vaccine to be considerd it must
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-target must be recognized as foreign
-response to epitopes -cell mediated and humoral response |
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T/F: Antibody to an antigen always results in neutralization of that antigen
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False
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A bacterial polysaccharide surface antigen vaccine are unable to provide affinity matural or class switching so, it requires __________ to work
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conjugation to carrier
(activate B cells to IgM, but no help) |
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Polysaccharide-protein conjugates in bacterial surface antigen vaccines improve immunogenicity by:
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-activate Thelper cells
-enable class switching (IgM to IgG) -activate memory B cells |
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An anti-idiotype vaccine may be used helpful for:
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-toxic antigens
-poorly immunogenic antigens -antigens difficult to purify |
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Toxin/toxoids vaccines are very effective but require ___1___. Toxoids are detoxified when treated with ___2__, adsorbed onto aluminum salt and thimersol added as a preservative
Why two toxoids are combined? |
1. boosters
2. formaldehyde 3. Tetanus and diptheria |
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How do recombinant vaccines work?
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-clone gene for antigen
-insert into cell (culture, yeast, animal) to produce large amount of antigen -insert gene for antigen into a non-virulent virus or bacterium -bacterium or non-virulent virus acts as a vector to infect host and produce antigen in situ |
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Problems with Recombinant vector vaccines
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-pre-existing Abs to vector
-resistance to vector infection -inflammation |
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_____ DNA is used ti increased potentcy and cellular response is needed for a recombinant vaccine. If use for gene for conserved protein, it can protect against multiple strains.
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Naked DNA. I have no idea what the fuck any of that means.
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Advantages/Disadvantages of a Killed / Inactivated Vaccine
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Advantages: cannot initiate infection,is polyantigenic, and adverse effects is local inflammatory response
Problems: Multiple doses necessary, Ab titers drop over time, |
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Polio, Rabies, Influenza, and Hep A vaccines are all example of what kind of vaccine?
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Killed/Inactivated Vaccines
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Danger of Live attenuated vaccines
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-immunocompromised
-adverse effects simlar to mild natural illness -can transfer agent to others -potential for wild type virulent strain |
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Poliovirus, MMR, and BCG for mycobacteria are all examples of what kind of vaccines
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Live attenuated vaccines
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Added to vaccine to increase immune response by increasing antigenicity and stimulating inflammatory response
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Adjuvants
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Phenomeneon where adjuvants concentrate antigen at a site where lymphocytes are to it and induce cytokine production
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depot effect
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How do adjuvants increase immune response
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-increase antigenicity
-inflammatory response -activate DCs through Toll like receptors -Depot effect -immune stimulating complexes -Multivalent vaccines |
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Adjuvant that delivers antigen directly to antigen presenting cell is known as _______ ____ ____
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Immune stimulating complex (ISCOMS)
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Why is a Rotavirus vaccine difficult to make? What issues did the previous one have?
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-different strains in different areas
-causes intestinal intussusception |
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-picornavirus
-fecal oral transmission (contaminated water) -ifnets motor neurons of the spinal cord resulting in paralysis -Inactivated and Live-attenuated (Sabin vaccine) |
Poliovirus
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Differences between Salk polio and Sabin vaccines?
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Salk: killed/ inactive, no IgA in nasal & GI
Sabin: live and attenuated with IgA but has shown wild type reversion |
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Problems with trivalent oral polio vaccine in developing country?
So what did they do? |
-Delivery system (cold chain required)
-Failure of vaccine to establish in kids with diarrhea -interference by other enterovirus (shitty water) mono therapy |
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-Orthopoxvirus (Poxviridae)
-dsDNA -no animal reservoir or human carriers -erradicated in 1970s -vaccinations stopped in 1972 -rash on face and extreminities, skin lesions |
Smallpox
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Vaccinia induced antibody for small pox was detected by day ___ post vaccination (primary). Secondary vaccination resulted in ______________
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10.
Classic delayed hypersensitivity |
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Eczema vacinatum causesvaccinial eruption and severe _____. Give vaccinia ______.
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inflammation
immune globulin |
