BIOM 250: Week 11,12
BIOM 250: Week 11,12 BIOM 250
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This 9 page Class Notes was uploaded by Davis Notetaker on Wednesday April 27, 2016. The Class Notes belongs to BIOM 250 at Montana State University taught by Kari Cargill in Winter 2016. Since its upload, it has received 15 views. For similar materials see Micro Hlth Sci: Infect Disease in Biology at Montana State University.
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Date Created: 04/27/16
Wed 4/20 Study showed Dyson brand hand dryers actually lead to ore potential spread of vaccines than paper towels News: Zika Virus emerging disease generating more concern as studies find it is easily transmissible through mosquitoes and even person to person via sexual activity Disease: Measles disease/infection Measles aka Rubeola etiologic agent Measles Virus (MeV) (caused by: name, type of m/o, Probably one of most contagious diseases on earth other characteristics) reservoir (where it is harbored naturally) mode of transmission to Respiratory transmission humans (& susceptible 90% of susceptible people contract the illness if exposed people) pathogenesis (progression of Complications disease within body, virulence ● Sinusitis, pneumonia ,encephalitis factors) ● Subacute sclerosis panencephalitis (SSPE) ○ 1 in 100,000 cases ○ Caused by virus persisting in the brain ○ 68 years after illness children would exhibit mental deterioration & death ○ highest risk if infected at younger than 2 years old ○ nearly always fatal if not caught early symptoms ● Fever ● Raised, red rash ● Koplik’s spots ○ Small, white spots inside mouth treatment/prevention/control Treatment: SSPE Antiviral drugs and interferon used if it is caught early enough Mortality rate: Developed countries < 1% Developing countries 1013%, even with existence of vaccine (estimated more than 450 deaths daily worldwide) Prevention: MMR vaccine (measlesmumpsrubella) 1963 Hilleman developed the 1st vaccine 9095% of a vaccinated pop achieves herd immunity Rubella aka German Measles ● Highly contagious ● Can be transmitted via nasal secretions ● 1969 vaccine developed ● Complications: congenital rubella syndrome Immune System Immune System has 2 branches 1. Humoral immunity antibodies found in fluids (blood, lymph, secretions) = “humors” i. Provides resistance to bacteria, viruses & toxins outside of cells b. B cell lymphocytes i. Develop in the one marrow (in humans) c. Plasma cells, which are mature B cell lymphocytes, who produce d. Antibodies that act against specific antigens 2. Cell mediated immunity (CMI) a. T cell lymphocytes i. Recognize antigens ii. T cells are developed in thymus b. Provides resistance to abnormal eukaryotic cells: i. Euk m/o’s e.g. fungi, protozoa, parasites ii. Intracellularlyinfected cells/phagocytes iii. New Organs transplant rejection 1. Rejection due to new organs with foreign antibodies iv. Cancer 1. overwhelms T cells Antibodies Are immunoglobulins (lg) These are protein molecules that recognize & bind to antigens Each antibody is specific to one antigen: Yshaped molecule w/ 2 antigenbinding sites that are specific to the antigen Classes of antibodies lgG (8085%) Majority of circulating ab lgG come from mothers: cross the placenta to protect the fetus IgM (510%) Pentamer 1st to appear w/ new antigen, but short lived Next exposure to the same antigen is generally responded to with mostly lgG IgA (15%) Secretory antibody found in secretions (e.g. saliva, sweat, colostrum, mucous membranes, breast milk) IgD (2%) not much is known about it IgE (.002%) responsible for allergic reactions Antigenantibody interactions ● Neutralize toxins (by blocking off the active site) ● Inactivate viruses & bacteria by preventing these from binding to host cells ● Agglutination (agab complex) can enhance phagocytosis by coating antigens ● Start complement actions (cause cell lysis) Friday 4/22 Active T Cells 1. Helper T cells (T H a. Stimulates other T&B cells to react to an antigen b. Mainly where HIV infections found 2. Cytotoxic T cells (T ) C a. Kills abnormal euk. Cells 3. Delayed hypersensitivity T cells (T ) D a. Attracts macrophages to specific location of concern b. Also triggers delayed allergic reactions Examples: Mantoux test Inject TB ag under skin If abs present reaction occurs Allergic contact dermatitis, eg latex, jewelry allergies Clonal Selection Theory ● Presence of a foreign antigen stimulates a specific response “selection” of counterspecific cell occurs ● Maturation of selected stem cells ● During presence of a foreign antigen, relevant cells become active B&T lymphocytes and “clones” of these are produced en mass SelfTolerance ● Elimination or inactivation of “antiself” B & T cell lines ● Occurs during fetal development ● If not: possibly leads to autoimmune disorders Monoclonal antibodies (mabs) Abs are very specific/unique, and this makes them a good tool for infection identification Ex: Hybridoma B cells interacting with tumor cells leads to production of hybridoma These generate antibodies commonly used for diagnosis (or therapy) Diagnostic Uses: rapid chlamydia test Uses antichlamydia abs Interacts with chlamydia ags (if present) and test indicates + Therapeutic uses: Humanized mabs (through a process of genetic engineering) ● Immune system suppressant: ○ Prevents transplant rejection ○ Can be used to treat allergic asthma, and in some cancer treatments Immunodeficiency Disorders Primary disorders genetic defects Secondary disorders infectious agents, leukemias, meds, radiation HIV/AIDS Acquired Immunodeficiency Syndrome (AIDS) Human Immunodeficiency Virus (HIV) ● Origin ~1908 in Central Africa: SIV trans to humans ○ Simian Immunodeficiency Virus (SIV) ○ thought to have been transmitted via monkey hunting in Africa ● 1980 AIDS first recognized as a disease ● 1983 HIV identified as etiologic agent HIV 2 types of HIV: ● HIV1 most common worldwide ● HIV2 mostly occurs in West Africa (less virulent) Subtypes HIV1 has 11 subtypes ● 90% of US cases are HIV1, clade B HIV Structure ● Ss RNA genome ● Reverse transcriptase enzyme “Retrovirus” ● Helical capsid ● Enveloped ● Spikes gp120 “glycoprotein” Retrovirus ● Reverse transcription ○ generation of complementary DNA (cDNA) from RNA ○ This is then incorporated into the host cell’s DNA Life Cycle 1. Attachment a. Susceptible cells are CD4 cells b. Virus gp120 spike “fits” the cell’s CD4 antigens and CXCR4 (or CCR5) coreceptor i. Individuals without this coreceptor can be exposed multiple times without contracting the disease 2. Penetration a. Virus envelope fuses with the cell membrane 3. Reverse transcription a. Provirus b. Latent at this point c. Reverse transcription process has a very high mutation rate: i. A person may have more than 1 million variants during the asymptomatic stage, and 100 million variants during the symptomatic stage 4. Biosynthesis a. Synthesis of proteins & RNA 5. Maturation 6. Release: via budding Disease Progression Group 1: HIV infection In the first few weeks an exposed person experiences: ● High viremia (highest level of virus in blood at this stage, an exposed person is most infectious at this stage) ● May have flulike symptoms Immune Response: ● Abs made (over a few weeks) ● Test will indicate HIV + at this stage ● Most virus already cleared from blood Group 2: Asymptomatic ● Provirus ● Still test HIV+ & can infect others Group 3: Symptomatic Early symptoms: ● Swollen lymph nodes, rashes, mouth ulcers ● Cd4 cell count decreases ● These symptoms occur after years Advanced symptoms: more severe ● Fever, diarrhea, weight loss ● Infections: thrush (yeast), shingles ● Precancerous lesions (rarely) Group 4: AIDS ● Avg ~ 10 years after initial exposure without treatment ● AIDS indicator conditions AIDS victims often have indicator diseases and/or conditions that show up due to weakened immune system ● In fact, most AIDS deaths are due to opportunistic infections Fri 4/22 HIV Propagation ● 100 billion HIV’s made daily ● Each virus only lives 6 hours ● Most of these are produced by CD4 T cells ● These T cells survive for only 2 days (they normally live years) ○ This has critical impact in the health of the host ● Every day, 2 billion CD4 T cells are made to compensate ● Net loss of 20 million cells each day HIV Testing 1. Antibody tests a. An infected individual may not have produced antibodies early in the infection, which will affect the accuracy/results of these tests i. Rapid blood test (does not require extensive lab time) ii. “Home” test card to hold blood drop is mailed iii. Oral saliva test iv. Urine test (less accurate) b. 20% of HIV infected people are unaware of being HIV+ 2. Viral tests a. Cost more money and requires more time HIV Transmission Via body fluids: ● Blood ● Semen ● Vaginal fluid ● Breast milk ● NOT: saliva, urine, sweat, tears ● NOT: insect vectors, casual contact, fomites (except intravenous needles) ○ HIV very fragile outside of host body ● Congenital transmission infants of HIV+ mothers ○ 2025% of the time transmission occurs ○ Infected infants have less than 18 months to live ○ Drug therapy minimizes transmission Prevention & Treatment ● Minimize transmission ● Antiviral drugs ○ Various modes of action: ■ Inhibition of reverse transcription ■ Protease inhibitors ■ Block CD4 antigens ○ Can extend lives by years ○ If caught early enough, daily use minimizes transmission ○ Issues with antiviral drugs: ■ Expensive ■ Toxic ■ do not cure patients, who are still infectious ■ some HIV strains are drugresistant ● HIV vaccine ○ Difficult to develop due to: ■ Too many virus variants ■ Uncertainty of how to deal with provirus ■ Ethical issues with testing ● Found vaccines lead to higher risk for contracting the disease ● Determined there were too many unknown factors about the virus to safely continue testing ■ Too many unknown factors ● Therapy ○ Complications or symptoms are treated ○ There is no cure Mon 4/25 & Wed 4/27 Movie: A Paralyzing Fear: The Story of Polio in America Under course reserves at MSU Library Disease: Polio disease/infection Poliomyelitis etiologic agent Poliovirus (caused by: name, type of m/o, S.s. RNA other characteristics) Enterovirus capsid reservoirwhere it is harbored humans naturally) mode of transmission to Fecaloral route humans (& susceptible people) pathogenesis (progression of ● Incubation ~335 days disease within body, virulence ● Poliovirus binds to CD155 receptor factors) ● This leads to viremia (virus in bloodstream) ● Virus circulates to other tissues and muscles, referred to as secondary viremia Complications: Virus enters CNS & replicates in motor neurons, causing temporary or permanent paralysis symptoms Viremia asymptomatic Secondary viremia Fever, headache, sore throat Paralysis, < 1% of cases Very rarely: respiratory arrest and death treatment/prevention/control Prevention: Vaccine several types ● Attenuated virus (first vaccine developed) ● Killed virus ● Live virus taken orally, generally used in developing countries due to ease of administering the vaccine Treatment: No cure, therapies focus on relieving symptoms Fri 4/29 Exam 4 Option
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