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MICR 4430 (3)
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Department
Microbiology
Course
MICR 4430
Professor
Sarah Wootton
Semester
Winter

Description
 Use of oral contraceptives for 5+ years LECTURE 10 – VIRAL INFECTIONS  Chemical nature of the HPV virus  Smoking  structure genome: dsDNA  High parity (5+ full term pregnancies)  Previous exposure to STD  size: 9kb  Range of lesions caused by HPV (e.g. from benign  Differences between high & low risk HPVs (e.g. warts to epithelial carcinomas) & types differences in the function of E6 & E7)  High risk HPV: anogenital cancers (cervix)  Benign lesions: HPV viral DNA exists as circular DNA in nucleus  HPV 16/18  Cancerous cells: HPV DNA integrated into  Low risk HPV: benign genital warts  HPV 6/11 host genome  Integration of DNA disrupts E2  Viral genes involved in transformation region, which is responsible for  E6 & E7: tumor suppressor proteins downregulating E6/E7 (oncogenes) (p53/Rb)  HIGH RISK E6/E7 binds to p53/pRb  E5: amplifies viral genome (upper layers  increased cell proliferation, epithelium) genomic instability, accumulation of  How early and late gene expression is regulated mutations = cancer during productive infection  LOW RISK E6/E7 bind weakly to  HPV genome  nucleus  3 regions: long p53/pRb  lower capacity to induce control region (LCR), early region (E), late malignant transformation region (L)  Changes in viral gene expression patterns that  LCR: regulates viral replication + accompany progression to cervical cancer controls transcription of some early  CIN1: similar to productive lesions genes  CIN2 & 3: onset of late events is retarded +  E1 & E2: viral DNA replication production of infectious virions restricted to  E4: amplifies viral genome (upper smaller area closer to epithelial surface layers of epithelium)  Cervical cancer: productive stages of virus  L1 & L2: viral capsid, expressed late life cycle no longer supported, viral in infection (upper layers of episomes lost epithelium)  Composition of HPV vaccine  The role of cellular differentiation of the cutaneous epithelium in the HPV life cycle  Gardasil: quadrivalent recombinant vaccine – mixture of VLP from L1 capsid protein of 1. Basal layer has lots of stem cells – HPV (6, 11, 16, 18) divides  L1 protein has intrinsic capacity to 2. While dividing, virus genome partitioned assemble into empty capsid-like into daughter cells  one of daughter structures cells detaches from basal layer  moves to stratum + differentiates  Most effective before sexual activity, 3. Infected cells that leave basal layer 100% effective against the 4 HPV types remain active in cell cycle because of  Cervarix: created using L1 protein of HPV E7 16/18 a. E7: retains nuclei throughout all  Noninfectious VLPs from infected epithelial (normal uninfected cells lose nuclei after Baculovirus leaving basal layer)  Higher generation of Ab than 4. Cell cycle involves shedding of Gardasil (2x more for HPV16/ 6x keratinocytes  releases HPV to infect more for HPV18) & 2x more B cells for both others  Chemical nature of the HSV virus e.g. structure 5. E6 + E7 dysregulate cell cycle + inhibit apoptosis genome, size, etc.  Strategies HPV employs to evade the immune  dsDNA 150kb/ enveloped system  How herpes viruses are classified – based on 1. Pap virus don’t infect antigen presenting location in latent state: 1. Alpha (Neuron) – HSV-1&2/VZV cells (APC) in epithelium 2. HPV don’t lyse keratinocytes 2. Beta (B lymphocytes) – CMV/HHV-6&7 3. Little opportunitiy for APC to eat virions 3. Gamma (mono/lymphocytes) – + derive antigens ABV/HHV-8 4. No blood-borne phase of infection  Stages/life cycle of HSV infection (e.g. following (immune system outside of epithelium infection of epithelium) has little opportunity to detect)  Clinical features of HSV-1, -2 infection  Factors important in the development of cervical cancer by HPV (e.g. HPV type, cofactors, etc.)  Both cause painful vesicle on skin, spreads from direct contact (saliva/genital secretions)  1: oro-facial lesions, universal  2: genital lesions  Primary infection  Silent infections, 1-3 days to appear  Recurrent disease  Mechanisms contributing to latency  LAT viral gene inhibits apoptosis + maintain latency by promoting survival of infected neurons  LAT produces miRNA that causes apoptosis resistance by downregulating transforming growth factor (TGF)-beta1 + SMAD3 expression LECTURE 11 - VIRAL HEPATITIS  Causative agents of viral hepatitis and their distinguishing biological characteristics including genome, virion structure and modes of transmission  Symptoms of viral hepatitis  The significance of markers in HBV infected patients and how these markers and the serological profiles differ in acute and chronic HBV infections  The significance of hepatitis delta virus (HDV)  Range of clinical outcomes of hepatitis B infection infection on the course of HBV infection and what determines whether an individual will clear  HDV = defective virus that needs HBV to the virus or remain chronically infected multiply  Higher chance of liver failure + progression to liver cirrhosis + liver cancer  Superinfection (chronic HBV + delta) causes more rapid/severe progression than co- infect (new HBV + delta)  Transmission of HCV and the role of the host response in the development of chronic HCV infection  Transmission: transfusion/transplant from infected donor, I.V. drug use, hemodialysis, accidental needle/sharps, sexual/household exposure, multiple sex partners, fetus transmit  Host response: alanine aminotransferase (ALT)  Acute: T cell responses present until HCV cleared & accelerated memory nd response with 2 infection  Chronic: T cells are weak, fail before virus is cleared  The composition of vaccines against viral hepatitis  Transmission: Bird-Mosquitoes LECTURE 12 – VIRAL ENCEPHALITIS  What is an arbovirus (Culiseta melanura) cycle  vridge  Aborvirus = arthropod-borne virus vectors (birds)  infect humans/horses (mammals)  Maintained in nature by biological  Mammals don’t circulate transmission between susceptible vertebrate virus in blood enough to hosts using blood-feeding arthropods infect mosquitoes  Zoonotic, nonhuman primary vertebrate hosts, undetected unless impacts human  Vaccine: none vector interaction, “dead-end” hosts Western equine encephalitis because don’t produce significant viremia or  Transmission: mosquitoes (Culex and Culiseta) contribute to transmission cycle, variety of **mainly in Canada vertebrate hosts, vertical transmission (egg-  No vaccine offspring)  Bunyaviridae  La Crosse encephalitis  Vaccines available  Causative agents of viral encephalitis  Major arboviruses that cause encephalitis  Flaviviridae West Nile virus  Transmission: 1. Infected mosquitos – feed on infected birds, spread to humans/animals 2. Transfusions/transplants/mother- to-child – rarely happens  Prevention: 1. Sprays – adulticides (Sumithrin) 2. Dead-bird reporting 3. Mosquito testing 4. Disease reporting 5. Blood supply screening St. Louis Encephalitis Virus (SLEV)  Most common mosquito-transmitted human pathogen in US, no vaccine/preventative drug  Transmission: Mosquitoes (Culex) feed on infected SLEV birds, spreads to humans/animals, grows in birds/mosquitoes but don’t make them sick Japanese Encephalitis (JEV)  Most common arboviral encephalitis worldwide  Transmission: Mosquitoes (Culex) in rice fields by feeding off infected pigs/wild birds, transmit to humans/animals Vaccines: none for most encephalitides  Togaviridae Eastern equine encephalitis (EEEV)  Criteria for eradication: no non-human LECTURE 13 – VIRAL SKIN RASHES  Causative agents of viral skin rashes and their reservoirs, sensitive + specific diagnostic general biological characteristics including genome tools exist, effective vaccine available and virion structure  Limitations to vaccine, so eradication is good  German measles (Rubella): togavirus,  Attenuated measles vaccine +ssRNA, enveloped  Measles virus: Paramyxoviridae, -ssRNA, inactivated by light/heat sphere + nonsegmented  Half potency lost after reconstitution  *** generalized maculopapular rash 3+ if stored at 20 C 1 hr, all lost at 37 C 1 hr days, fever of 38 degrees celcius,  Vaccine must be injected cough/runny nose/conjunctivitis  Measles virus pathogenesis including clinical subcutaneously/intramuscularly (the symptoms and immune response to infection use of needles is important)  Two stages: initial stage – runny nose,  Vaccine isn’t as efficient on maternally acquired antibodies and cough, red watery eyes, small white spots immature immune systems (infants) on cheeks (Koplik’s spots) – after several days: caulopapular rash develops on face +  Attenuated measles – potential of upper neck, eventually reaches hands and serious lung/brain infection in feed (lasts 5-6 days and fades) immunocompromised  Measles rash, Koplik’s spots,  **ideal measle vaccine: inexpensive, safe, heat-stable, immunogenic in infants, single conjunctivitis dose, no needle  Pathogenesis 1. Initial infection from respiratory tract  Poxvirus pathogenesis and course of clinical  Spreads to local lymph nodes disease (pulmonary macrophages)  other 1. Incubation period (7-17 days, not contagious): no symptoms lymph nodes  spleen  viremia --. 2. Initial symptoms/Prodrome (2-4 days, Epithelial surface  virus deposits itself at oropharynx, conjunctiva, sometimes contagious): fever, malaise, skin, respiratory tract head/body ache 3. Early Rash (4 days, MOST contagious): small red spots on tongue, sores that break open + spread large amounts of virus into throat/mouth, starts on face + spread to arms/legs, rash becomes raised bumps with thick, opaque fluid 4. Pustular Rash (5 days, contagious): bumps become pustules, firm and sharp raised 5. Scabs (5 days, contagious): form a crust  scab 6. Resolving scabs (6 days, contagious): scabs begin to fall off, person is contagious until all scabs fall off 7. Scabs resolved (not contagious) pitted scars left  The significance of “vaccinia virus” & vaccination advent  Vaccinia: vaccine virus for small pox  Jenner used cowpox to vaccinate a  Immune response boy, later challenged with VV   Early innate response: MV induce protected IFN-alpha & IFN-beta & NK cells  Variolation: administration of  Antibodies: first detectable when material from known smallpox cases rash appears (IgM)  switches to to protect recipients IgG which is love avidity but  Small pox eradication increases slowly  No reservoir for VV but humans  Cellular immunity: CD8T cells activated + expanded during MV  Only causes acute infections that infection  CD8T cells immunity can cause either: death or recovers with life-long immunity established after infection  MV  Vaccinia virus is effective antigens … -_- immunogen  Measles virus eradication  Pathogenesis of VZV infection  Varicella-zoster virus (VZV)  Primary infection with VZV by respiratory epithelial cells (gains access to highly permissive Tcells in tonsil lymphoid tissue)  Incubation p
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