Viruses and Exam 4 – Flashcards
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| Definition of a virus Define viron |
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| Virus =organized association of macromolecules-nucleic acid within a protective shell of protein units Viron = new intact infectious virus particles that consist of nucleic acid core with a protein coat sometimes with external envelopes that is the extracellular infective form of a virus. |
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| What are some arguments for viruses being organisms? |
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| Can replicate Have evolution Independent in terms of not being limited to single organism or host |
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| What are the basic building blocks of a virus? |
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| -nucleic acids -proteins (structural and non structural) -carbohydrates (part of the envelope) -lipids (in envelope) |
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| Describe the structural and non structural proteins in viruses |
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| Structural = viron proteins which protect the genome, have ligands for cell receptors. Nonstructural= enzymes to regulate replication -transcriptases -reverse transcriptases -integrases |
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| What are the simplest viral structuresWhat kind of symmetry exists? |
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| Helical (rod structure) Icosahedral (12 capsomers with 5 fold symmetry, 20sided). Has 5:3:2 symmetry Can also be icosadeltahedrons (soccer ball) or more complex shapes. |
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| How do capsid viruses assemble? |
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| Individual proteins made from host's materials (capsoid material) associate into subunits, then protomers, capsomers, and finally a procapsid or capsid. Self-assembly is helped by molecular chaperones made inside the host. |
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| Define capsid -what is function of capsidDefine envelope What is VAP? What is it on a capsid virus and an enveloped virus? |
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| capsid= outer layer of viron, very resistant and rigid. -function= packaging or condensation, protect nucleic acid, transport nucleic acids, specificity of attachment. envelope= membrane composed of lipids, protiens, and glycoproteins that cannot survive harsh conditions. VAP= viral attachment protein -capsid=part of capsid or protein extending from capsid -enveloped=glycoproteins on the envelope |
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| What is an enveloped virusWhich viruses are enveloped? |
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| A virus that acquires an outer lipoprotein coat by budding off the host cel membranes. All of the (-) strand RNA viruses are enveloped. |
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| What is hemagglutinin (HA)What do mutations here causeWhat is Neuraminidase (NA)? |
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| HA= VAP, spike shaped trimer that can also bind erythrocytes and mediate viral attachment. Mutations here cause minor drift and major shifts in antigenicity. NA= glycoprotein tetramer with enzyme activity to facilitate release from infected cells. |
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| Name the steps in viral replication |
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| Recognition of target Attachment Penetration Uncoating Macromolecular synthesis -early mRNA transcription and protein synth -replication of genome -late mRNA with structural protein synthesis -post-translational modification of protein) Virus assembly Budding of enveloped virus Release of virus |
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| What are the host immune responses directed against? |
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| Viral antigenic epitopes |
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| How does a virus infect a cell? |
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| it either injects nucleic acids into cell and leaves ghost behind Or enters via inducing host endocytosis. |
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| Name the three ways a virus can replicate genetic info inside the host cell. |
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| 1) Viral DNA is replicated along with host DNA 2) RNA replicase copies viral RNA and uses that as a template to make many duplicates. 3) Use reverse transcriptase to make complementary DNA from RNA. Then go to protein. |
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| What is a provirus or prophageWhat is lysogenic bacteria? |
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| When viral DNA is incorporated into host chromosome in a latent infection. Provirus in animals/plants Prophage in bacteria Lysogenic bacteria= bacteria which contain latent prophages in their DNA. can be awakened by UV radiation or chemicals. |
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| What are Early, Late, and Lytic proteins? |
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| Early = enzymes used in nucleic acid replication Late= proteins used to construct virus coat Lytic= proteins used to break open cell for viral exit |
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| Generally describe the lytic cycle |
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| Phage attachment, injection of DNA into host, replication of DNA by host, manufacture of viral DNA by host, virus self-assembly and bursting out of cell. |
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| What is the tegument? |
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| Between the capsid and the envelope Ill-defined layer of proteins |
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| What are 5 ways to name a virus? |
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| 1) describe characteristics 2) describe members of it's family 3) describe body sites where it was isolated 4) describe disease it causes 5) describe locations it was isolated |
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| Name some characteristics of Enveloped viruses What are the consequences of these characteristics? |
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| Components are membrane lipids, proteins, glycoproteins Tissue tropism (host specifcity) Buds through cell membrane, often associated with chronic and persistent infection Environmentally unstable, susceptible to physical and chemical forces. Causes seasonal diseases. Consequences= must stay wet, can't survive GI, don't need to kill cells to spread, droplet spread, need CMI+humoral for protection. |
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| Name some components of Non-enveloped viruses What are the consequences of these characteristics? |
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| Contains only nucleocapsid protein Environmentally stable, resistant Lytic infections, acute disease Year-round and non-seasonal disease Consequence= easily spread by fomites, can dry out and retain infectivity, survive GI, Humoral immunity is enough for protection. |
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| What is viral attachment? |
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| Attachment= binding of VAPs on surface of viron to receptors on the cell |
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| What is viral tropism? What helps determine it? |
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| Tropism is ability to replicate in particular cells or tissues. Determined by receptors on host cells interacting with viral VAP. |
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| How does a non-enveloped virus penetrate the cellEnveloped virus? |
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| Non-enveloped= endocytosis or viropexis Enveloped= fusion and endocytosis |
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| Where does replication occur for DNA viruses? what is the exception Where does replication occur for RNA viruseswhat is the exception? |
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| 1) DNA viruses replicate in the nucleus using host's enzymes to make mRNA >exception is poxviruses that must encode all own enzymes RNA viruses replicate in cytoplasm and must code all needed enzymes themselves >exception is orthomyxovirus and retrovirus |
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| Properties of DNA virus replication |
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| DNA can stay in infected cells stably and establish persistent infection. Replicates in nucleus. (except poxvirus) Viral genes interact with host transcriptional machinery (except poxvirus). Host DNA polymerase needs a primer for viral genome replication. Smaller the DNA virus the more dependent it is on the host cell. Larger viruses have more control over the replication of their genomes. |
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| Properties of RNA virus replication |
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| RNA is labile and transient Replication is in cytoplasm Must code a (+) strand or carry an RNA-dependent RNA polymerase Prone to mutation due to lack of proofreading Genome determines mechanism of transcription >Plus strand, minus strand, ambisense, retrovirus. |
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| How can specific receptor binding be side stepped in attachment phase of virus infection? |
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| By antibody coated virus particles binding to Fc receptors on monocytes which results in virus uptake. |
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| Is viral attachment reversible? |
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| Yes, but elution from the cell often leads to changes in virus which decrease or eliminate possibility of attaching to other cells. |
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| What does the capsid of poliovirus consist of? Describe these components and what they do. |
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| VP1, 2,3,4 VP4-buried in capsid and associated with RNA VP1,2,3 form external capisd. Five VP1 protein subunits form a canyon which is recognition site for receptor. |
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| Describe the uptake of poliovirus into the host cell |
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| Binds to polio receptor and is endocytosed into an endosome. At low pH the virus is lipophilic and can form a pore in the endosome. During this, VP4 and VP2 are lost from particle to increase flexibility. RNA is injected into cell via the endosomal pore. |
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| Describe uncoating for the following viruses Reovirus Poxvirus Othromyxo, paramyxo, picornavirus Influenza Herpes, adeno, papova viruses |
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| Reovirus- capsid partially disintegrates and replication takes place in structured particles Poxvirus-host factors induce disruption, DNA release depends on viral factors made after entry Orthomyxo, paramyxo, picorna=lose envelope or capsid upon entry Influenza=M2 protein allows endosomal protons into viron particle; dissolution/ permit replication Herpes, Adeno, Papova=capsid routed along cytoskeleton to nuclear envelope |
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| Name examples of the following virus types -dsDNA -ss(+)DNA -dsRNA -ss(+)RNA -ss(-)RNA -ss(+)RNA, DNA intermediate -dsDNA, RNA intermediate |
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| -dsDNA (adeno, herpes, pox) -ss(+)DNA (parvo) -dsRNA (reo, birna) -ss(+)RNA (picorna, toga) -ss(-)RNA (orthomyxo, rhadbo) -ss(+)RNA, DNA intermediate (retro) -dsDNA, RNA intermediate (hepadna) |
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| What is an inclusion? |
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| Inclusion=accumulation of virions at sites of assembly, visible in stained cells with light microscope. |
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| Describe budding |
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| capsid proteins and nucleic acid condense next to the cell membrane. Viral-coded envelope proteins are introduced into the cell membrane and concentrate near these aggregates. Mambranes surrounding the nucleocapsid then bulges and nips off to form new enveloped virion |
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| Define antigenic drift and antigenic shift and what they mean for viral antigenicity. |
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| Drift = where individual in the sequence mutate. These are small changes and results in changed antigenicity. Shift = occurring via recombination or reassortment. A major change in the viral genome. |
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| What type of viral genome is more stable? |
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| DNA virus genome is more stable. RNA viruses tend to mutate more because of lack of proof reading |
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| Define the following types of mutations Point Deletion Insertion Frame shift |
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| Point = changes in a single nucleotide base Deletions = total removal of genetic information either on a large or small scale. Insertion = extra DNA is added into an existing gene Frame shift = adding or subtracting one or two bases resulting in a shift of reading frames. |
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| Define Recombination What kind of virus does this commonly? |
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| Recombination = exchange of chromosomes from two different genetic sources, typically from the same species. Occurs commonly in DNA virus or RNA virus with a DNA phase. |
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| Define Reassortment What kind of virus does it occur in? |
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| Mixing of genetic material of two similar viruses that are infection the same cell (co-infection). Occurs in viruses with segmented genomes. |
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| Define oncogenic virus and name a few examples |
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| DNA virus that is associated with human neoplasia. (Some RNA viruses can cause tumors also but in animals) Human papillomavirus Hep B and C EpsteinBarr virus Human T-lymphotropic virus |
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| How do oncogenic viruses cause cancer? |
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| 3 ways 1) Presence of viral DNA disrupts host DNA function 2) Viral proteins affect normal host gene regulation 3) Virus serves as a vector for oncogene insertion |
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| Define viral complementation |
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| When two viruses interact at the functional level and use each other's proteins to assemble a new progeny. |
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| Define defective virus Define Defective Interfering Viruses (Di) |
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| Virus that lack the gene that lets them complete the replication cycle. A "helper" virus must be present to help it completely replicate. Can either be related or unrelated. Di= virus that decreases replication of helper virus by competing for precursors etc... May change course of infection. |
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| Where do DNA viruses replicateWhere do RNA viruses replicateWhat are the exceptions? |
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| DNA virus replicates in nucleus. Exception is poxvirus which replicates in the cytoplasm RNA virus replicates in the cytoplasm. Exception is orthomyxovirus and retrovirus which we didn't talk about |
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| What is an infectious naked genome? |
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| DNA viruses (except poxvirus) and (+) RNA viruses (except retrovirus) where nucleic acid is sufficient to initiate replication upon injection in to cell. |
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| What are the properties |
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| What is responsible for the self-limiting nature of most viral infections? |
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| Host defense mechanisms! So you don't have to treat most viral infections, just wait until the defenses take care of it. |
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| What do Non-immune Defenses include? |
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| 1) innate immunity (anatomic and chemical) 2) cellular resistance (cells that lack factors for viral replication 3) inflammation (limits the spread) 4) interferon (inhibits viral replication) is first defense mechanism induced by virus 5) RNAi (interfering RNA) binds to viral mRNA and inhibits gene expression. |
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| How does humoral immunity work against a viral infectionWhat do neutralizing antibodies do? Non-neutralizing? |
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| Neutralizing and non-neutralizing antibodies against viral specific antigens. Most important against cytolytic viral infections. Neutralizing Ab inhibit ability to attach, penetrate, or uncoat. Or all three. Non-neutralizing enhances phagocytosis of viron degradation as opsonins or to attract complement. |
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| How does cell-mediated immunity work against viruses? |
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| Tc, Ab dependent cell mediated cytotoxicity, NK cells, and activated macrophages. This is most important against non-cytolytic infections where the membrane on infected cell is antigenically altered. |
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| What can cause viral induced immunopathology? |
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| Immediate hypersensitivity Ab-Ag complexes Tissue damage due to cytotoxic cells or Ab-complement. |
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| What is viral-induced immunosuppressionWhen does it occurWhat does it involve? |
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| Altering of immune responsiveness or decrease in number of lymphocytes Occurs with either cytolytic or non-cytolytic infections. Seen often as consequence of diseminated viral infections that involve lymphocyte infection. |
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| How do you treat a viral infections? |
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| Immuno therapy (before infected) Antiviral Interferon |
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| How would you diagnose a viral infection? |
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| 3 basic approaches in lab 1) virus isolation 2) direction demonstration of virus, nucleic acid, or antigens in clinical specimens. 3) serologic testing of viral specific antibodies. BUT clinical symptoms are usually distinct so lab tests frequently not needed. Just good history and physical exam. |
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| How would you Isolate Viruses in the lab(live, fixed, and eggs) |
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| Identifies virus replication in susceptible cells. 1)in live infected cells look for cytopathogenic effect (CPE): polykarycyte formation, hemadsorption, cell death 2)In fixed infected tissue culture cells look for inclusion bodies or stain for viral Ag. 3)In embryonated egg look for pock formation (blood vessels that are dark on the egg) |
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| What is indicative of a viral infection for paired blood sample testing? |
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| One anti-viral antibody titer taken at onset and one at recovery phase. Fourfold increase in titer must be present to indicate infection. |
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| What is a virus neutralization test? |
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| Constant amounts of virus are incubated with decreasing amounts of serum added to susceptible cells. Based on principle that certain antiviral antibodies neutralize the CPE of the virus. |
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| What is the hemagglutination inhibition test? |
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| Anti hemagglutinin antibodies in serum will inhibit viral agglutination of erythrocytes. Positive reaction makes clumps with WBC. |
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| What is a solid phase immunoassay |
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| Use viral antigens in RIA and ELISA protocols. Sensitive and specific assays used to find certain viral antibodies. |
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| What is influenza? Define transmission, incubation periods, commuincability, and timing. |
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| Influenza=respiratory infection Transmitted by contact with respiratory secretions from infected person. Incubates 1-5 days from exposure to onset Communicable 1-2 days before until 4-5 days after Sx onset. Peak occurs December through March in North America. |
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| Describe Sx of influenza |
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| Fever-sudden, 38-40 deg C x 3-4 days HA, aches and pains Mod-exteme weakness Bedridden 5-10 days max Sometimes runny nose and sneezing Chest discomfort usually, can be severe Complications of respiratory failure |
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| Name some complications of the flu |
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| Pharyngitis, croup (harsh cough, hoarse, fever) in kids, otitis media, pneumonia, Secondary infections by strep pneumoniae, staph aureus, hemophilus influenzae. Myositis (rare), cardiac complications, encephalopathy, liver/CNS involvement (Reye syndrome), Buillian-Barre syndrome. |
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| What is histological mechanism behind flu-induced pneumonia? |
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| Destruction of cilia in respiratory epithelium causes decreased clearance. Basement membrane damage results in loss of protection. Both increase risk of bacterial secondary infection. |
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| Who is at risk for the flu? |
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| >65 years old pt with chronic diseases infants and kids <2 yo pregnant women nursing home residents |
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| What family is influenza inWho do the different types infect? |
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| ssRNA virus of Orthomyxoviridae family. Type A: animals and humans of all ages, causes epi and pandemics Type B: humans only, mostly kids. Milder epidemics. Type C: swine reservoir but human associated outbreaks, milder disease. |
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| Describe the structure of influenza virion |
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| M1 protein underneath lipid bilayer, most abundant protein. Genome organized in 7-8 segments. Integral membrane proteins that coordinate fusion are NA, HA, and M2. Helical nucleocapsid is ssRNA plus NP protein (important for subtyping). NS protein important for virulence. |
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| What is Hemagglutinin? |
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| antigenic glycoprotein found on surface of flu viruses (and others) Has ability to cause erythrocyte clumping in vitro. |
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| What is Neuraminidase? |
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| Glycoside hydrolase enzyme found on surface of influenza virus (and others) and is a surface antigenic glycoprotein. |
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| Antigenic shift of influenza What is itHow oftenWhat type does it? Whats the mechanism? |
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| -phylogenic evolution that accounts for emergence of new strains of virus and potential for epidemics or pandemics. Results in immunologically distinct novel H/N combinations. -every 10-40 years -Type A only observed one to do it. -Genetic reassortment between circulating human and animal strains is responsible for this. |
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| Influenza antigenic drift What is itHow oftenWhat typesWhat mutations are most meaningful? |
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| -Minor changes in antigenic character -occurs every 2-3 years -mutation rate for type A is highest and lowest for type C -most meaningful mutations are in HA1 protein. |
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| Pandemic influenza What is itTransmission type Describe |
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| -any global outbreak of a novel influenza type A virus subtype -person to person transmission -associated with very high rates of morbidity and mortality. Has multiple waves of disease occurring 4-6 months apart. |
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| Why hasn't H5H1 become a pandemic yet? |
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| Avian flu (H5N1) hasn't been able to efficiently transmit human to human yet. It also hasn't entered the Western Hemisphere yet. |
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| What population had the highest death rat in human bird flu cases? |
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| 90% infected under 40 years of age. Death rate highest among age 10-49 (76&) Age 50 and over had lowest (40%) Under age 5 (44%) Age 5-9 (49%) |
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| What is the WHO framework INTERPANDEMIC PERIOD? |
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| Interpandemic period Phase 1: no new flu subtypes detected in humans. If in animals, infection risk is low. Phase 2: No new flu detected in humans. But animal flu subtype substantial risk of human infection. |
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| What is the WHO framework PANDEMIC ALERT PERIOD? |
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| Phase 3: human infection with new subtype but no human to human spread, or rare. Phase 4: small clusters with limited inter human transmission, localized. Phase 5: larger clusters but inter human spread still local. Substantial pandemic risk. |
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| What is WHO PANDEMIC PERIOD? |
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| Phase 6: increased and sustained transmission in general population |
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| What defines the POST PANDEMIC PERIOD? |
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| a return to interpandemic period (phase 1 and 2) |
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| What is the transmission and incubation for H1N1? |
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| Human to human Exposure to coughing/sneezing or fomite Unknown incubation. Could be 1-7 days but more likely 1-4 days Infectious period unknown. Could be 1 days prior to 7 days post onset. Children may be infectious for up to 10 days. |
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| What was the age group most infected by H1N1? What was the age group with most mortality by H1N1? |
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| 1st - 5-24 years 2nd - 0-4 years 1st - 25-49 years (41%) 2nd - 50-64 years (24%) |
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| How do you prevent flu infection? |
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| Only proven method is yearly vaccine. Killed virus injection 2 weeks before flu season begins. |
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| What does the flu vaccine consist of? |
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| 2 influenza A viruses and 1 B virus. It's trivalent. |
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| Is the nasal vaccine with live attenuated virus the same as the shot? |
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| Yes. You get the same effect. The spray is likely to cause mild upper respiratory Sx but not more likely to cause fever, chills, or weakness. |
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| What is the global surveillance network? |
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| 200 WHO laboratories in 79 countries and 4 coordination centers. During the year flu virus samples are sent to these centers and they make recommendations on the strains expected next year for the vaccines. |
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| What are some ways to test for flu (labs), how long do they take, and how common are they to use? |
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| Culture (1-10d)-still gold standard RT-PCR (2-4hrs)-becoming gold standard Ag Detection (2-4hrs)-needs expertise and IF microscope Serology(>2wks)-more retrospective, needs paired sera Ag Detection/rapid EIA-like (15-30min)-widely available |
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| What are some drugs used in influenza? |
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| Zanamivir (for A and B) Osteltamivir (A and B) Amantadine (A) Rimanadine (A) But really best way is through prophylaxis via vaccine. |
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| What are some challenges in managing flu patients? |
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| -enough beds but not enough ventilators -staff shortages -limited ability to call on external resources -magnitude and duration |
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| What was the first anticancer vaccine? |
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| Hepatitis B vaccine because it reduced incidence of HBV related childhood hepatocellular carcinoma by 75%. |
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| Who developed tests specific to Hep C virus? |
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| Houghton et al. in 1989 |
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| What is route of transmission for Hep A and E? |
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| Fecal oral route. They do not exist in chronic carrier state. |
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| What is route of transmission for Hep B, C, and DWhat forms do they have? |
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| Parenteral transmission Both acute and chronic forms Chronic form serves as carrier state. |
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| Hep A: How many genotypes identified for humansWhat ethnic group has highest rates of diseaseWhat is inbucation periodWhere does replication occur? |
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| -4 human genotypes (I-VI), infection with one confers immunity to others. -Native Americans, select Hispanic, migrants -15-50d (mean 30d), excreted in stool for 1-2wks prior and 1wk after onset. -replicates only in the liver |
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| Hep A What age ranges get jaundiceHow high is mortality rates? |
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| -unusual in kids <4yo -4-6 yo 90% anicteric (no jaundice) -older than 15yr 40-70% get jaundice Self limiting virus rarely causes death. |
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| World wide, how many HBV carriers are there and now many die each year? |
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| 350 million carriers 500,000 deaths [er year |
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| How does one become a carrier for HBV? |
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| In endemic areas, occurs at birth. 90% births progress from acute to chronic infection of HBV. 20-50% aged 1-5 become chronic. Chances of chronic infection decrease to <5% in adults. |
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| Who is at risk for HBV? |
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| Prevalence of infection among blacks is 4x that seen in whites. Followed by Hispanics and whites. |
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| How is HBV transmitted? |
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| cutaneous and mucosal exposure to infectious blood or bodily fluids. In US it's contaminated needles and syringes or multiple sex partners. |
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| What is the hallmark of HBV infection? |
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| HBsAg which appears in the serum during the incubation period (usually 1-10 weeks after exposure and 2-7 weeks before Sx onset) |
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| What other viral infection is closely related to HBV infectionWhat are the subtypes? |
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| HDV Type I - US and Europe; increased risk of fulminant course or rapid progression to chronic liver disease Type II - East asia Type III - South America; Yucpa Indian outbreaks. |
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| What are the clinical manifestations of HDV infection? |
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| Varies. B9 acute hepatitis to fulminant liver failure. Chronically may get asymptomatic carriers or may progress faster to cirrhosis and hepatocellular carcinoma. |
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| What are 2 scenarios of acute infection with HDV? |
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| Co-infection with acute HBV Super-infection in chronic HBV pts |
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| What causes majority of HCV infectionsHow can it be distinguished from other hepatitisFewer than 15-25% of causes of acute HCV infection result in _____? |
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| Injection drug use but >40% have no reason. Only by serological testing. Jaundice. There is high rate of subclinical infection. |
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| What is incubation for HCVWhat are some Sx? |
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| Mean is 50d -fatigue, poor appetite, R upper quad pain, low fever 2-10d -serum sickness-like syndrome (rash, urticaria, and arthralgias) |
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| When is HCV RNA detectable in serum? |
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| Within days to 8 weeks post infection. |
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| Which heptatitis is associated with high incidence of chronic disease? |
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| HCV (85%). There is absence of Sx. Can persist in silent fashion for decades until finally manifests with end-stage liver disease. |
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| Who do you screen/ who is at high risk for HCV? |
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| -pts who are at high risk for infection -pts who exhibit fatigue, poor appetite, and/or wasting. |
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| What is replacing the term STD? Many of above do not result in ____and are ___ |
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| STI replacing STD Many STI do not result in disease and are asymptomatic |
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| What are modes of acquisition for HSVWhat percent of US adult popluation have symptoms? |
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| -sexual contact with infected person -transfer to fetus or new born from infected mother. -10% of US population have symptoms. |
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| What is risk of infection to uninfected partner for HSVWhat is the break down of types? |
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| -75%! -80% with HSV-2 (below waist) -20% with HSV-1 (above waist, cold sore) |
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| What is the most common infection which can lead to genital ulcers, most people are undiagnosed due to mild infections, and can be acquired by sex with asymptomatic person? |
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| HSV |
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| What is the risk of infection from mother to child of HSV? Mortality rate? |
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| Risk is 30-50% chance of transmission (1 in 20,000 deliveries) -mortality rate for babies who acquire it during vaginal delivery=60-70% |
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| What is HSV incubation period and symptoms? |
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| Incubates for 2-7days Initial local pain, tenderness, pruritits, and dysuria. Profuse watery vaginal discharge may occur. Papular lesions on an erythematous base which develop into vesicles then breakdown into ulcers covered with grayish exudate. |
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| Name the vesicle locations on male and female HSV infections. |
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| Female- labia majora and minora, vaginal mucosa, cervix, perineal region Male - glans penis, prepuce, shaft of penis |
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| What is pathogenesis behind persistence HSV infections? |
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| During primary infection pt has viremia and regional lymphadenopathy. Then HSV invades local nerve endings and ascends the sacral ganglia. Following shock to immune system, virus replicates in sacral ganglia, travels down axon, and causes recurrent lesions in epidermis. |
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| In most pts, recurrent lesions heal within a ______period of time than lesions that occur during primary infection. After primary infection, Sx are_______. |
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| Shorter Not as severe. |
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| How do you diagnose HSV clinically and in the lab? |
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| Clinic - presence of vesicular lesions and sexual Hx. Lab - virus cx, positive Tzanck test, immunostaining lesion cells, serological testing to G1/G2 glycoproteins in HSV-1/2 |
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| When is therapy for HSV indicated? How effective is it? What are the limits? |
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| Antiviral therapy during episodic recurrences may shorten DURATION of lesions. Suppressive antiviral therapy can prevent or shorten recurrent outbreaks. Rarely you give IV antiviral Tx during severe diseases. Does NOT cure or prevent viral latency!!! |
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| When does asymptomatic shedding occur most frequently? |
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| -in pts who have had genital HSV-2 infection. AND in those pts who have genital herpes for >12 months. |
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| What is the national prevalance for HSV-2? Race? Gender? |
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| Nationally 16.2% African Americans 39.2% Black women 48% |
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| What is the clinical appearance of HPV? |
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| -can have venereal warts (condyloma acuminata): moist, soft cauliflower bumps within 3wk-8mo on cervix, labia, vulva, perineum, penis, urethra, scrotum. Painful, friable, or pruritic. |
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| What are the features of HPV-6 and HPV-11? |
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| -most common cause of genital warts in US (most common STI) -causes warts only and rarely associated with SCC. |
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| What are the features of HPV-16 and 18? |
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| -it's DNA found in 85% of cervical carcinoma, believed to be major cause of invasive cervical carcinoma. Found in 60-90% cases of penile carcinoma. |
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| What is the incubation period for genital warts? |
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| 3-4 months. HPV6 and 11 may recede spontaneously |
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| How do you diagnose HPV? What is a definitive DX? |
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| Clinical: biopsy, 3-5% acetic acid on cervix or penis reveals aceto-white epithelium of HPV-16 and 18, PAP smear to look for koiloctosis in cervix Definitive=viral nucleic acid or capid proteins in samples taken from cervix or penis. |
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| How do you treat HPVWhat happens if you dont? |
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| Removal of warts: cryotherapy excision, laser, chemical cautery. Recurrence several months after treatment is common because there is no cure! -no change in wart, spontaneous resolution, increase in size/# |
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| How do you prevent HPV? |
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| -avoid contact -use condoms -quadrivalent vaccine for 6, 11, 16, and 18 in females aged 9-26. |
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| HPV and cervical carcinoma epidemiology Risk of cervical cancer_____related to age at first intercourse. Risk of cervical cancer____related to lifetime number of sex partners. |
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| Risk is inversely related to age at first intercourse. Risk is directly related to lifetime # sex partners. |
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| HIV-1 is found_____ HIV-2 is found_____ |
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| Worldwide West Africa |
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| Which HIV is more potent? Which is more closely related to monkey HIV |
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| HIV-1 is more potent. HIV-2 is less and related to monkey HIV |
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| What is most common mode of transmission for HIV world wideWhat is it in US? |
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| Worldwide it's HETERO contact In US its MSM contact, with women being infected the most via HETERO contact. |
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| What race has highest prevalance of adults living with HIV in the US? |
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| Males>females Blacks, Hispanic, Indian/White, Asian |
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| -What is the worldwide leading cause of death for people infected with HIV-How old is the average HIV pt in the US? |
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| -TB -males aged 30-44 years. in populous cities. |
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| What population is in most need of HIV testing? |
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| MSM: white first, then hispanic, and blacks. Older than 30 men were unaware of their infection. |
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| Who is less likely to know their HIV status? |
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| Young MSM and MSM of color. 1 in 5 MSM in 21 US cities has HIV But 44% are unaware. |
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| How does income affect HIV status? |
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| 2.1% heterosexual living in high poverty urban areas are infected |
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| What are common modes of HIV transmissionWhat is the most common in the US? |
answer
| Anal, vaginal, homosexual, heterosexual, transfusion of blood, needle sharing, mucous membrane exposure among health care workers, needle stick, open wound, tattoo needles. Transplacental, peripartum, breast milk ingestion. (at birth and through milk is most common for <5 yo) Most common is male homosexual routes. |
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| What are screening tests available for HIV? |
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| ELISA-> can detect 3-4 weeks after infection. Need 2 different tests to be positive for initial screen. Then need western blot to be confirmed. 97% develop Ab in 3 months. Rarely takes up to 6 months to develop. RT-PCR used during 2-4 weeks of infection when pts are seronegative but still infective. Can also be used to confirm Tx efficacy. |
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| How do you determine if a neonate is infected? What are the complicationsHow can you prevent neonatal infection? |
answer
| Do an ELISA test. Ab from infected mother can cross the placenta making Dx using serology impossible. So use RT-PCR instead. Don't breast feed the baby. Pregnant women should go on anti-retrovirals. |
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| What is part of the standard care for HIV screening? |
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| -make HIV testing routine part of medical care -all pts betwee 13-64 should be tested at least once regardless of risk factor -high risk pts tested annually. |
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| What are the stages of untreated HIV? |
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| Stage1: incubate 1-3 weeks, ends with production of high titers of Ab @ 2-3 mo post infection. Stage2 Stage3 |
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| What are the Sx of stages 1? |
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| Can have NO sx or the following: low grade fever, myalgia, arthralgia, lymphadenopathy, hepatosplenomegaly, HA, meningitis, encephalitis rash |
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| What are Sx of stage2 HIV? |
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| -usually asymptomatic -can persist for 6 yrs or longer, large amounts of Ab produced -virus detectable in blood, semen, and cervical secretions -Sx if there=persistent generalized lymphadenopathy or AIDS related complex. |
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| What are the Sx of AIDS related complex? |
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| fever, fatigue, diarrhea, weight loss, night sweats, immunologic abnormalities, dementia, spontaneous neoplasms. |
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| What are the Sx of stage 3 HIV infection? |
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| Various opportunistic infections or neoplasms begin Severity and frequency of above is directly related to decline of CD4 T cells. |
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| What is the diagnosis of AIDS consist of? |
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| <200 T cells per microliter of blood Clinical Dx of category C conditions (candida and other fungal infections, mycobacterium infection, recurrent pneumonia, toxoplasmosis of brain, wasting syndrome, viral encephalopathies, kaposi sarcoma) |
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| What does HIV therapy consist ofGoals of therapy? |
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| -life long tx to suppress virus -Highly Active Antiretriviral Therapy (HAART) has good result but complex Tx plan. 1) fewer opportunistic dz means longer lifespans for pts. 2) suppress viral replication and halts damage to immune system 3) partially restore immune system with partial restoration of function. 4) strongly correlated with reduction of new HIV in population. |
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| How many classes of antiretrovirals are available and how many combos for HAART? |
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| 5 classes of anti-retrovirals 3 combos of HAART |
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| What is the goal of immunization? |
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| -produce humoral Ab against pathogen -produce Ab against toxin -make T cells that provide cell mediated immunity |
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| What is passive immunity? How can it be acquired? |
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| -immunity without immune system being challenged. via transfer of serum of gammaglobulins both natural or artificial. |
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| Give some examples of natural and artificial passive immunity |
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| - natural: mother to fetus through placental transfer IgG, colostral transfer of IgA -Artificial: transfer by injection with gammaglobulins from animals or other people. |
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| What is active immunity? What are the 2 types? |
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| -immunity produced by the body following exposure to antigens. (like vaccines) -Naturally acquired=exposure to various antigen leads to subclinical infections which results in protective immune response. -Artificial=immunization may be via giving live attenuated pathogens or dead ones or their components. |
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| Define and give examples of... 1)Live vaccines 2)Killed vaccines 3)Sub-unit vaccines |
answer
| 1)virus has lost pathogenicity but still infectious (measles, mumps, only bacterial is BCG vaccine against TV) 2)Bacteria has been killed through heat, chemicals, or UV radiation (cholera, pertussis, plague) 3)purified cell wall components or viral particles (Hep B, Hib, pneumococcus) |
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| What are side effects of immunizations? |
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| fever, malaise, discomfort @ injection site. Joint pain (rubella), convulsions (pertussis), neurological disorders (flu) Allergies to eggs with vaccines made in eggs. Serious effects documented after DTP vaccine but that was eliminated. |
