MCB Exam 4 – Flashcards
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Unlock answersT/F: Most viruses are smaller than 0.45 nm, so are detected by electron microscopy. |
True |
______________ is the inactive form of a virus. Once inside host it becomes active. |
Virion |
What are the general virus characteristics? |
1. Sub-Microscopic 2. Obligate intracellular parasite 3. Host specificity 4. Needs host 4 energy n protein synthesis
|
List the components that make up the virus structure. |
1. Nucleic acid 2. Capsid 3. Envelope 4. Spikes |
T/F: Not all viruses have to have nucleic acids. |
False; all must have it! |
What is the function of the virus capsid? |
1. Protects DNA/RNA against damage 2. Involved in recognizing the host surface 3. Facilitates nucleic acid penetration
|
What 2 structures must all virus have? |
Nucleic acids Capsids |
What are virus envelops composed of? |
Host lipids and viral proteins |
What are virus spikes used for? |
Recognition and attachment to host |
What types of infection can occur with virus? |
1. Lytic = kills host 2. Persistant = small amounts of virus, host lives 3. Transforming = changes genetics, causes cancer 4. Latent = hides in host, no effect on host |
What are some of the ways the virus damages the host? |
1. Cell lysis 2. Cell transformation can lead to cancer 3. Produces toxic products 4. Alters host structure such as nuclear or cytoplasm |
What is the major virulence factor for viruses? |
The presence of the virus in the cell |
What are some ways that viruses can entry into host tissues? |
1. Directly by trauma or insect bite 2. Thru mucous membranes of the resp. tract or alimentary tract. |
Where is the most common entry site for viruses? |
Respiratory tract |
Define viremia |
When the virus reaches the blood system |
What are some of the reasons why viruses are able to grow inside hosts? |
1. Fast action 2. Adapts to host biochemical conditions 3. Able to resist host defense mechanisms |
Describe the virus replication cycle. |
1. Attachment 2. Penetration 3. Un coating 4. Provision of energy 5. synthesis of Low MW compounds 6. Nucleic acid and protein synthesis 7. Assembly 8. Release |
What are some ways the virus evades the immune responses of the host? |
1. Inhibits the MHC I restricted Ag Presentation so no CD8 response 2. Inhibits MHC II restricted Ag presentation so no Ab, or Ag memory 3. Downregulates CD4 (T-helper cells) 4. Inhibits NK cell lysis 5. Intereferes with apoptosis 6. Evasion of humoral immunity 7. Inhibits cytokine action
|
List the different types of virus-cell interactions. |
1. Permissive or productive infection 2. Abortive or non-productive 3. Persistent 4. latent 5. Cytopathic effects (CPE) |
During permissive (productive) infection, the virus is produced and some cells are infected due to _____________. |
Receptors |
This type of virus-cell interaction leads to entry of the virus but no further expression occurs after a few genes are turned on. |
Abortive or nonproductive infection |
Which virus-cell interaction leads to the production of few viruses from few cells. Most the cells are infected but they do not die. |
Permissive |
During this virus-cell interaction, the virus does not produce itself. Rather it hides within the host. |
Laten infection |
The virus-cell interaction that you can visually see under the microscope are CPEs. What things can you see? |
1. Plaque formation in phage 2. Nuclear/cytoplasm enlargement 3. Nucleus changes 4. Cell fusion, syncytia formation 5. Lysosomes leaking 6. Viral budding, fibroblast 7. Changes in membranes |
What are the stages of the One - Step Growth cycle of the virus? |
1. Attach/adsorb to the cell 2. Penetration by fusion or endocytosis 3. Eclipse period 4. Rise = virus particles are detectable |
What is the Eclipse period of the One-Step Growth cycle of a virus? |
A phase in the proliferation of viral particles during which the virus cannot be detected in the host. Penetration, uncoating, and synthesis occurs here. |
Define receptor mediated endocytosis. |
Once the virus is inside it attaches to a clathrin coated pit and forms a coated vesicle. It now requires a low pH to cause fusion of virus to endosome and uncoats to release the virus. |
T/F: Some viruses use cellular transcriptase and some use viral transcriptase. |
True |
Define viral syndrome. And give some examples. |
It is the pathogenic manifestations of a viral infection.
1. Flu like and systemic symptoms 2. Infection of the eye, oral, resp. tract 3. Gastroenteritis 4. Hepatitis 5. STDs 6. Hemorrhagic fevers
|
What is the difference between cytopathology and immunopathology? |
Cytopathology = Branch of pathology that studies and diagnoses diseases on the cellular level.
Immunopathology = Branch of medication that deals with the immune response associated w/the disease. It includes the study of the pathology of an organism, organ system, or disease w/ respect to the immunity/response. |
T/F: Rubella is caused by cytopathology. |
False; it is not cytopathic (CPE) so the infection does not end in cell lysis. |
How many different types of Hepatitis are there? Which is considered to be Serum Hepatitis? What about Infectious hepatitis? |
A = Infectious Hepatitis B = Serum Hepatitis C D E |
These forms of Hepatitis are transmitted via percutaneous and permucosal. |
Type B, C and D |
These forms of Hepatitis is transmitted via fecal-oral route. |
A and E |
Which types of Hepatitis virus can lead to a chronic infection? |
B, C, and D |
Out of all the Hepatitis types, which is ones do not have a vaccine available to it? |
Hepatitis C and E |
Which types of Hepatitis are associated with liver cancer? |
Hep. B and C |
This type of Hepatitis has a reverse transcriptase, DNA Poly. and RNAse H. Also has ds and ss DNA and is in an enveloped icosahedron. |
Hep. B |
What are the modes of transmission for Hep. B? |
1. Sexual 2. Parenteral injecting 3. Perinatal |
Where is the [M+] of Hep. B the highest in the body? |
In blood, serum, wound exudates |
How can you prevent Hep. B? |
1. Prevent perinatal HBV transmission 2. Routine vaccines for all infants 3. Vaccinate |
Hep. C is in the _______________ family and has _________________ genome. |
Flaviviridae +ss RNA |
How is Hep. C transmitted? |
1. Blood transfusions 2. IV drug users 3. Sex |
T/F: Only Hep. B is associated with liver cancer. |
False; Hep. B and C are associated with liver cancer |
What does Percutaneous and permucosal mean? Both Hep. B and C undergo this type of route of transmission. |
Percutaneous 1. Injecting drug use 2. Transfusion 3. Contaminated equipment 4. Needlestick 5. Clotting factors b4 viral inactivation
Permucosal 1. Perinatal 2. Sexually |
Which route of transmission of Hep. C is the most common? |
Injection from drug users |
What are some nosocmial transmission of Hep. C? |
1. Contaminated equipment 2. Unsfae injection practices such as multiple dose medication vials |
When does perinatal transmission of Hep. C occur? |
Only when women HCV-RNA positive at delivery
(higher incidence in HIV women) |
T/F: Men to men is the more effiecient sexual transmission of Hep. C. |
False; male to female transmissio more efficient. (indicative of sexual transmission) |
Which type of transmission of Hep. C accounts for 15-20% of acute and chronic infections in the U.S. Also serves as a large chronic reservoir that provides hihger risk. |
Sexually transmitted |
Can household transmission of Hep. C occur? If so provide an example how? |
Yes, it can. Sharing contaminated razors, toothbrushes, etc. |
How can you prevent Hep. C? |
1. Avoid direct exposure to blood 2. Cover cuts and sores on skin 3. Do not share items that may have blood on them 4. Do not donate blood, body organs, etc |
T/F: Hep. C can be transmitted by kissing. |
False; not spread by kissing, hugging, sneezing, coughing, sharing utensils |
What are some ways to prevent sexual transmission of Hep. C? |
1. Use condoms 2. Limit # of partners 3. Get vaccinated against Hep. B
|
What can remove the envelope of Hep. B? |
Alcohol |
Out of all the Hep. types, which one is considered to be a retrovirus? |
Hep. B It has reverse transcriptase |
Provide an example of a contaminated equipment and unsafe injection practice that contribute to the nosocomial transmission of Hep. C. |
Contaminated equip = Hemodialysis
Unsafe injection = plasmapheresis |
What 2 drugs when co-administered together help to treat Hep. C? |
Interferon and Ribavirin |
What are important features of Hep C transmission via injecting drug use? |
1. Hihgly efficient amoung injection drug users 2. Rapidly acquired after initiation 3. 4x more common then HIV 5. Prevalence 60-90% after 5 years |
Ribavirin is a analogue of ___________, with an incomplete base ring and an available 3'-OH grp. |
Guanosine |
What are the sites of activity for Ribavirin? |
1. Inhibits nucleoside biosynthesis 2. Inhibits capping of mRNA 3. Inhibits RNA Poly. |
Which Hep. (B or C) has more cases of symptomatic infections?; Which has the most cases of death from chronic liver disease? |
Sympt = B (70K-160K; vs 3K- 54K) ; Liver = C (8K-10K vs 5K-6K) |
Describe the Herpes Virus structure. |
1. Enveloped icosahedral capsid 100 nm 2. 9 Glycoproteins 3. 30 structural proteins, but codes for 120 4. Tegument is amorphous 5. No common family antigen |
What are the 3 subfamilies of Herpesviridae? |
1. Alphaherpsesvirinae 2. Betaherpesvirinae 3. Gammaherpesvirinae |
Subfamily Alphaherpresvirinae include which 2 genus? What;virus does each genus include? |
1. Genus Simplex virus = HSV1 and 2, B virus 2. Genus Varicella virus = varicella-zoster virus (chicken pox) |
The subfamily Betaherpesvirinae includes these 2 genus? |
Genus Cytomegalovirus Genus Roseolovirus |
What genus does the human herpes 6 and 7 belong to? |
Genus Roseolovirus |
Which subfamily of Herpres includes the genus Lymphocyrptovirus? And is associated with the Epstein-Barr virus? |
Subfamily Gammaherpesvirus |
The herpes virus had ___________________ DNA and naked DNA is ____________. |
Double stranded linear infectious |
AlphaHerpes is _____________-tropic BetaHerpes is ________________ tropic Gammaherpes is ______________-tropic |
Neuro Salivary gland Lympho |
Describe the multiplication cycle of the Herpes virus. |
1. Attachment - glycoproteins on viral envelope fuses with cell P.M. 2. Penetration - direct or endocytosis 3. Envelopes are acquired at inner nuclear membrane 4. Virions are released by reverse phagocytosis 5. Cell is not killed, but the functions are taken over by the virus |
When does latency of the Herpes virus occur? |
With persistant infected cells in which no infectious virus is formed because the multiplication cycle is stopped at some stage. |
What are some characteristics of;HSV1? |
1. Fever blisters 2. Occurs early in life 3. Primary infection is 8-10 days 4. Latent infection is asymptomatic ; |
In HSV1 where does the viral DNA reside? |
In the sensory ganglia |
When do recurrent infections occur in HSV1? |
When the virus replicates and travels down the nerve fiber to infect epithelial cells. |
HSV2 is sexually transmitted. Where does the virus reside during latency? |
In the nerves of the lower back (sacral plexus) |
When does recurrent infections occur in HSV2? |
5 or more times per year |
T/F: Prego women cannot transmit HSV2 during childbirth. |
False, they can |
List the viral syndromes caused by HSV1. |
1. Encephalitis 2. Keatoconjunctivitis 3. Pharyngitis 4. Esophaitis 5. Gladiatorum 6. Oral 7. Genital 8. Whitlow |
List the viral syndromes caused by HSV2. |
1. Meningitis 2. Oral 3. Pharyngitis 4. Genital 5. Perianal 6. Whitlow |
When it comes to the brain, HSV1 causes ________________whereas HSV2 causes ____________________. |
Encephalitis Meningitis |
What are some major characteristics of the Varicella-zoster virus? |
1. Spread by resp. tract 2. Chicken pox = seasonal epidemics 3. Vesicular rash w/systemic infection 4. 2-2 1/2 wks long infection cycle 5. More severe in adults 6. Recurrent infection occurs |
Recurrent infections of varicella-zoster virus is called ___________ and is localized to a ___________. |
Shingles Specific nerve |
What are some major characteristics of Cytomeglavirus (CMV)? |
1. Infects and causes no obvious disease 2. Prego can abort fetus 3. Transmitted by saliva 4. Virus secreted in milk, saliva and semen 5. Major problem in immunosuppressed peeps |
A primary infection of the EBV causes ________________and ________% of people over 40 carry this virus. |
Mononucleosis 95% |
Which herpes virus family member causes cancer? |
HHV-8 is associated with Kaposi's sarcoma in AIDS patients
EBV is associated with Burkitt's lymphoma in AIDS patients and related w/ nasopharngeal carinoma in Africa |
What does Togaviridae mean? |
Covered virusees |
What are the 3 genera associated with Togaviridae? Which is the cause of german measles? |
1. Alphavirus 2. Rubivirus = causes Measles 3. Arteriviruses |
Unlike other togavirus infections, Rubella causes a _____________ and can spread by ________. |
Respiratory illness Aerosols |
T/F:; There is an insect vector with Rubella. |
False; none |
Why is Rubella dangerous to prego women? |
If mom does not have Ab to Rubella virus (from prior infection or vaccine), then virus can replicate in placenta and spread to fetal blood supply. |
What are some syndromes associated with congential infection of Rubella? |
1. Cataracts 2. Mental retardation 3. Deafness |
What are some important features of Paramyxoviridae family of viruses? |
1. Encased by a fragile lipid envelope 2. Nonsegmented (-) sensed ssRNA w/ 6-10 genes separated by noncoding termination, polyadenylation and initiation signals. 3. Replication occurs in the cytoplasm ; |
During viral replication of the family Paramyxovivridae, what does the virion attach to and how? |
Attaches to sialoglycoprotein or glycolipid receptor by the envelope glycoprotein |
Which 2 membrane glycoproteins are key to the pathogenicity of all paramyxoviruses? |
1. H, HN or G = glycoproteins mediate cell attachment 2. F(fusion) protein;= has 3 functions |
What do the envelope glycoproteins H, HN stand for? |
H = Hemagglutinin HN = Neuraminidase |
What are the 3 functions of the F (fusion) protein in all paramyxoviruses? |
1. Enables virus; to fuse to cell to form syncytia 2. Enable viral penetration by fusion of viral envelope w/ P.M. 3. Allows direct intercellular spread by cell to cell fusion (can now evade the bodys circulating Ab's, and allow transfer of infectious nucleocapsids to nearby cells) |
What is the body's cellular immunity response to paramyxoviruses? |
Elicite a neutralizing Ab that inhibts adsorption of virus to cell receptors, thus inhibiting the infection.; |
What occurs after 6 days with Measles? |
Virus spreads to all epithelial surfaces from the local blood vessels. (Viremia) |
What contributes to the respiratory damage, fever and early symptoms seen with Measles? |
The immune system |
What immunity/vaccine is there for Measles? |
1. Natural immunity against reinfection is effective 2. Passive immunization for the unimmunized (administer IgG) 3. Live vaccine |
T/F:; Severity of measles is affected by young age, low socioeconomic status and malnutrition. |
True |
List some complications that can occur with Measles. |
1. Subacute Sclerosing Panencephalitis 2. Subacute Measles Encephalitis 3. Acute Postinfectious Measles Encephalitis |
Why is Subacute Scelrosing Panencephalitis (comp. of Measles) fatal? |
Manifests years after acute disease and fatal because of the slow spread of the virus into the brain. |
Why does Subacute Measles Encephalitis occur only in immunocompromised children? |
Becuase there bodies fail to eliminate virus-infected cells as the body lack cytotoxic T cells. (CD8) |
Out of the 3 Measles complications that can occur, which is the most dangerous affecting 1 in 1000 older children. With a fatality of 15%.? |
Acute Postinfectious Measles Encephalitis |
How are Mumps transmitted? |
By saliva or other respiratory fluids |
What are some clinical features of Mumps? |
1. Distorted face 2. Edematous enlargement of the salivary glands 3. Infants often asymptomatic or as a resp. infection. |
What complications can occur with Mumps? |
Mumps Encephalitis that can result in unilateral nerve deafness |
_____________________ provides protective levels of the Ab by a single injection for at least 90% of those injected over a 20 yr period.; This decreased Mumps by 98%. |
MMR vaccine |
What are the common features of families in the order Mononegavirales? |
1. Non-segmented, (-) sensed ssRNA 2. Helical nucleocapsid 3. Virion associated RNA-dependent RNA Poly 4. Similar gene order 5. Single 3' promoter |
Which families are classified within the order Mononegavirales; which means they have common features of it. |
Filoviridae = Ebola Paramyxoviridae = Measles, mumps Rhabdoviridae = Rabies |
What is some important features of the rabies virus? |
1. Can infect all warm blooded animals 2. Causes acute, contagious infection of the CNS 3. 100% fatal once symptoms show 4. Occurs worldwide except Hawaii, Japan, Great Britian and smaller islands |
What are the principles rabies hosts today? |
Wild carnivores and bats infected with several virus variants |
What are the vectors of transmission of the rabies virus? |
1. Bite/scratch of an infected animal (99% of cases worldwide) 2. Aerosol transmission from a bat 3. Tissue transplants from infected human (eyes) |
T/F: There is no viremia with the rabies virus. |
True |
What is the course action of the rabies virus in humans? |
1. Enters vody and travels w/in neurons to the CNS 2. Causes encephalitis in the brain 3. Virus travels down the nerves and multiplies in many diff. organs
|
Which glands are the most important in the spread of the rabies virus from animal to humans? |
Salivary glands |
What are some symptoms of Rabies? |
1. Early = nonspecific includes fever, headache, tiredness, etc 2. Progesses = Insomnia, anxiety, confusion, paralysis, hallucinations, hypersalivation, hydrophobia, hard to swallow 3. Late = Delirium, coma, Death |
Which is the most definitive means of dignosis of Rabies? |
Virus cultivation |
What vaccines are available for Rabies? |
1. Preexposure Prophylaxis 2. Postexposure Prophylaxis |
Who should get the preexposure prophalyaxis for Rabies? |
Labworkers, vets, wildlife officers, animal handlers (people at high risk) |
Preexposure prophylaxis for Rabies is an ____________ immunization with cell culture vaccine. |
Active |
Which human disease is the only one that can be prevented by postexposure vaccination? |
Rabies |
How many does of HDCV should be given for PEP of Rabies and prompt administration of what? |
5 doses Admin Rabies Immune Globulin |
________% mortality if treatment is given before onset of symptoms associated with Rabies virus. |
0% |
What non-pharmacological treatment seems to reduce the spread of the Rabies virus. |
Thorough wound cleansing |
What family does the Rotavirus belong to? |
Family Reoviridae |
What are some important features of the Rotavirus? |
1. Wheel shaped, 70 nm 2. 2 concentric icosahedral capsids surrounding an inner core 3. dsRNA, 11 segments each coding for a viral protein 4. Non-eveloped |
Why is the Rotavirus hard to make a vaccine for? |
It has 6 serogroups (A-F)
Group A is the most common in humans |
What is the pathogenesis of the Rotavirus? |
1. Infects intestinal cells and kills them 2. Initial infection most severe 3. Absorptive surface of intestine is reduced 4. Fluid accumulation in lumen = diarrhea 5. Disease is self limiting 6. Dehydration problems |
Which Ig is protective against Rotavirus? |
IgA in colostrum (breast milk) |
A Rotavirus infection stimulates which Ig's? |
Secretory IgA Neutralizing IgG |
T/F: Maternal IgG is protective against Rotavirus. |
False; no protection |
What is the route of transmission for Rotavirus? |
Fecal-oral (highly contagious) ; Can survive for hrs on hands and days on surfaces! |
What are some clinical features of the Rotavirus? |
1. 1-3 day incubation period 2. May be asymptomatic 3. Mild to severe 4. Death due to dehydration and electrolyte loss 5. Fever, vomitting, watery diarrhea 6. Lasts 3-9 days |
What is the common treatment for Rotavirus? |
Oral Rehydration - glucose, H2O, electrolytes If severe, IV fluid replacement |
What is the most common cause of gastroenteritis in children? |
Group A Rotavirus |
How can you prevent Rotavirus? |
1. Good hygiene 2. Chemical disinfections 3. Breast feed newborns 4. Vaccinations* |
What is the problem with the vaccine RotaShield for Rotavirus? |
Blocks the intestine (intussusception) |
This vaccine is 98% protective against severe Rotavirus gastroenterisits.; It is a live oral vaccine. |
RotaTeq Vaccine |
What 3 syndromes can the Influenza virus infection cause? |
1. Uncomplicated Rhinotracheitis 2. Respirtatory viral infection followed by bacterial pneumonia 3. Viral pneumonia |
What are some major characteristics of the flu virus? |
1. Higher death in young and old (decline in cellular immunity) 2. Binds to clarithin coated pit--forms a coated vesicle 3. Needs a low pH to cause fusion to endosome and uncoat 4. RNA replication occurs in cytoplasm then to nucleus |
What is the mechanism of action of Amantadine and Rimantadine to treat Influenza virus? |
1. Ion channel blockers that inhibit the replication of influenza virus by targeting M2 protein 2. Block acidifications of endosomes which inhibits the fusion 3. Since no fusion, release of viral RNA is prevented |
What is the mechanism of action of Tamiflu against Influenza virus? |
It is a neuramindase inhibitor designed to attack the structures of the Influenza viruses A and B, preventing the spread of the virus w/in the body. |
What are some general characteristics of Piconaviruses? |
1. Small ~ 30nm 2. Naked icosahedral = Infectious 3. ssRNA 4. (+) sensed 5. Replication occurs in cytoplasm 6. Can go directly into cell and be translated |
What are some important features of enteroviruses? |
1. Stable at pH 3 so can survive passage thru stomach 2. Spreads by fecal oral route 3. Multiplies in cytoplasm 4. Produces a large precursor protein that can undergo post tranlational cleavage 5. Cause variety of diseases |
What is ICAM-1? |
Intracellular Adhesion Molecule-1 |
What is ICAM-1 role in virus attachment to the host? |
It is a specific cellular receptor that the Rhinovirus family attaches to. |
What is the difference btwn primary and secondary viremia? |
Primary = initial spread of virus in the blood from the the first site of infection
Secondary = Primary viremia that now affects organs such as the skin, brain, muscle, liver, & meninges |
What happens during Poliovirus replication? |
1. Adsorption to specific receptors 2. Internalization in vesicles 3. Lowering of the pH in the vesicles 4. Exposure of Hydrophobic grps on the virus |
List the 4 stages of polio virus infections. |
1. Alimentary phase 2. Lymphatic phase 3. Viremic phase 4. Neurological phase |
What is a major illness of poliovirus infection progression? |
Meningitis (stiffness of neck or back) Can lead to paralysis |
What is IPV? OPV? |
Inactivated Polio Vaccine Oral Polio Vaccine |
What was used to the kill the polio virus to use in the inactivated polio vaccine? |
Formaldehyde |
Which one (IPV or OPV) does not produce nasal and duodenal IgA protection? |
IPV |
What is Post-Polio Syndrome? |
Peeps who survived polio show muscular weakness and paralysis many yrs after infection and recovery.
|
How does Post-Polio Syndrome develop? |
Caused by death of individual nerve terminals in the motor units that remain after the initial polio attack. Maybe due to possible deterioration of nerves that are required to function for damanged nerves. (degeneration of motor neurons) |
Which type of meningitis is more common? |
Viral |
List the viruses that cause viral meningitis. |
1. Measles 2. Mumps 3. Enterviruses (Polio, Cox B and Cox A7/9) 4. HSV |
T/F: Viral Meningitis is more severe than bacterial and recovery is almost none. |
False; recovery is almost always complete and is less severe. (the above describes Bacterial) |
How is Viral Meningitis spread? |
By coughing, sneezing and poor hygiene |
Can you use antibiotics for viral meningitis treatment? |
No |
Is there a cure for Post-Polio Syndrome? |
No, can treat the symptoms such as muscle weakness |
By the end of 2007, how many people had HIV? How many died? |
33 million had it 2 million died from it |
What are the clad, groups, and subtypes of HIV? |
Groups= M (Major) N (Non-O/ Non-M) O (Outlier)
Clads = A, B, C, D, H, G, J, K
Subtypes = look at figure |
How can HIV be transmitted? |
1. Sex 2. Inoculation of infected blood/blood products 3. Mother to child |
HIV enters via mucosal linings during sexual contact, the first cells to become infected are ___________________. |
Mucosal Dendritic cells (MDC) |
Can you transmit HIV during nursing, if it is infected milk? |
Yes Transmission can occur before, during or after birth |
What is the likelihood of infection after a single exposure for the 3 routes of transmission of HIV? |
Sex = 0.01-1.0% Blood Transfusion = >90% Mom = 12-50% |
Globaly, which route of transmission has the highest frequency although it is the least efficient route of transmission? |
Sexual contact. Likihood after 1st exposure = 0.1-1%, but globaly accounts for 65-80 (73%) % of all cases |
Which route of HIV transmission is the most effective? |
Blood transfusion. >90% likelihood of infection after single exposure |
Which type of heterosexual transmission is the greatest? |
2x-5x risk from male:female>> female:male |
What are some features of the HIV structure? |
1. Reverse transcritpase that converts ssRNA to dsDNA 2. Has integrase that allows it genome to get into host DNA 3. Viral envelope proteins 4. Has a viral core w/proteins (M protein, Capsid, Nucleoprotein) 5. Accessory proteins |
What immune response occurs during the primary infection, clinical latency, Symptomatic stage of an HIV infection? |
Primary = Slight increase in the # of CD8+ T cells in wk 6, but returns back down by wk 9. CD4+ T cells decrease Anti-gp120 dramatically increases from 0.
Clinical = CD8, CD4 and Anti-gp stay fairly the same, hence the latency. This occurs for ~ 6yrs
Symptomatic = Slight decrease in Anti-gp, Decrease in 1/2 # of CD8 Dramatic decline in CD4 in 2 yrs. By year 8 nearly 0 CD4 T cells. This is when AIDs will develop |
After how many years of HIV infection, will AIDs develop in? What is nearly 0? |
After 8 yrs CD4 T cells are nearly 0 at this time. |
What is the pathogenesis of HIV? |
1. High turnover of HIV and infected CD4 T cell loads 2. Persistant Immune activation 3. Destruction of host immune system |
What is persistant immune activation that occurs with HIV infection? |
Exhaustion and death of immune cells |
What 4 symptoms of an acute HIV infection did he say to remember? |
1. Fever 2. Lymphadenopathy (enlarged lympth nodes) 3. Pharyngitis 4. Rash |
During which clinical stage of HIV, has the highest plasma vRNA, Infectious particles, and infected PBMC? |
During the Acute infection vRNA = 5 x 10^6 IP = 2,500 HIV-PBMC = >30,000 |
According to the CDC, a CD4+ T amount of < _____________ is classified as having AIDs. |
400 |
Describe the replication cycle for HIV. |
1. Adsorption to specific receptor 2. Penetration 3. Reverse transcriptase 4. vRNA transit 5. Integration into host DNA 6. Transcription 7. Transcript processsing 8. Translation/ Post translational processing 9. Capsid assembly/ budding 10. Capsid processing |
Which steps of the HIV replication cycle can therapy work on to prevent the disease? |
1. Antibodies to prevent attachment 2. Fusion Protein inhibitor 3. RT Inhibitors, so cant make viral DNA 4. Integrase inhibitor so cant incorportate viral DNA into host DNA 5. Protease inhibitors so no posst translational processing 6. Zinc finger inhibitors to stop capsid assembly and processing |
What is important about Anti-HIV nucleoside Analogs? |
They look similar to the nucleotides so they get incorporated into the DNA, but they dont function properly. They prevent further elongation of the vDNA. |
How do Non-nucleoside reverse transcriptase inhibitors work? |
Directly bind to the enzyme and interefers with the enzyme functions. Cant convert to viral dsDNA. |
What is HAART? |
Highly Active Anti-Retroviral Therapy
Many anti-HIV drugs to treat HIV+ peeps. Usually includes 1 NS Analog, 1 protease inhibitor and a non-nucleoside RT inhbitor or another NS analog |
What precursor does viral protease create? What things arise from this precursor? |
Gag-Pol precursor
Capsid Matrix Nucleoprotein Protease RT Integrase |
What precursor arises from a cellular protease during HIV post translational processing? Then what things can that precursor make? |
Env Precursor
Surface Env Transmembrane |
What do HIV protease inhibitors do? |
They prevent the HIV protease from cleaving the Gag-Pol precusor polyproteins into the individual viral structural proteins (capsid, matrix, nucleoprotein) and viral enzymes (RT, PR, IN) |
What evaluations should be performed before starting treatement for HIV? |
1. Complete history and physical 2. CBC and chemistry profile (include transaminases and lipid) 3. CD4+ T cell count 4. Plasma HIV RNA measurement |
What are the goals of HIV therapy? |
1. Maximal and durable suppression of virus load 2. Restoration or preservation of immunologic function 3. Improvement of quality of life 4. Reduction of HIV related morbidity and mortality |
________________ uses probes to detect selected mutations that are known to confer drug resistance. |
Genotyping Resistance tests |
___________________ measures the ability of the virus to grow in various concentrations of antiretroviral drugs. |
Phenotyping Resistance Tests |
Why is it important to thoroughly evaluate an HIV patient before starting treatment? |
To decide whether or not treatment is needed. If has a/symptomatic AIDs then treat. If Asymptomatic HIV then treatment should be offered (CD4 200-350). If CD4 > 350 w/ RT-PCR > 55K then varies on treatment option. Now have >30% chance of getting AIDs. If CD4 >350 but RT-PCR <55K then many would defer treatment. |
What are the major reasons for treatment failure in HIV patients? |
1. Resistance to drug = 70% 2. Low Drug [M+] at the viral replication site = 25% 3. Progressive decline of the immune system |
What are causes of treatment regimen failure in HIV peeps? |
1. Patient factors such as age, co morbidities, etc 2. No compliance, miss clinical appts 3. Drug side effects and toxicity 4. Pharmacokinetics factors such as metabolism is fast, food/fasting, drug-drug interactions, etc 5. Potency of antiretroviral regimen |
When does resistance occur for the following drugs that treat HIV? NRTIs = Nucleoside RT Inhibitors PIs = Protease inhibitors NNRTs = Non nucleoside RT Inhibitors |
NRTIs = 6-12 months PIs = 2-3 months NNRTIs = days-weeks |
When do you change an antiretroviral regimen for suspected drug failure? |
When 1 or more of the following occur: 1. Incomplete virologic response (failure to decrease HIV RNA) 2. Virologic rebound (Re-appearance of viremia after suppression. Shows resistance) 3. Immunologic failure (Persistant decline in CD4 T cell count) 4. Clinical failures (deterioration after 3 mo) |
What is the global distribution of HIV-1 subtypes? |
Highest cases were in Sub-Saharan Africa (Accounts for 70% of all cases and about 58% of all women in Africa have it), SE Asia and South America. In 2003, the global total = 40 million have it and 3 million deaths from it and 5 million new infections.
|
Why is it so difficult to develop a vaccine for HIV? |
RT is a high error prone enzyme that causes many mutations thus variations. The disease can spread by many different routes. There are many different Clads and subtypes of HIV, hard to make 1 that fits all. All have diff. properties/genes |
What is important about AZT? |
It is a nucleoside analog. So it looks like regular NT but instead of 3'OH it has a N3. This causes chain termination so no further elongation of viral DNA. |
What is important about RT? |
It is the viruses reverse transcriptase. This allows ssRNA to become dsDNA that way it can then go into the hosts DNA. |
What stage of HIV infection has the highest titer of virus? |
Acute (Primary) infection |
During which stage does persistant immune activation occur? |
During the Primary infection where your body is constantly trying to fight off the virus |
What is cross resistance? |
If develop for resistance to 1 drug then become resistant to other drugs that have a similar mechanism of action (ex. if in same drug class) |
Which HIV drugs has the highest frequency of cross resistance? |
NNRTI > PIs > NRTI |
What is meant by Acute Fulminant Hepatitis? |
Acute liver failure |
Which Hepatitis virus causes Fulminant Hepatitis? |
Hep B.
(I'm not too sure, Hep A has 100 deaths a yr from this and Hep D has 35 deaths a yr. But Hep B is 150 deaths a year). |
Which herpes virus is more problematic for AIDS patients? |
Herpes Simplex |
What are the 2 main routes by which enteroviruses may reach blood? |
1. Fecal oral route (ingested) 2. Respiratory
(I'm like 90% positive about this) |
Once an enterovirus is in the blood, where does it go after that? |
Can go to the CNS and affect the brain. Or can cause secondary viremia and affect other organs such as the skin, liver, muscle. |
What is the % of people who previously had Polio will develop Post Polio Syndrome? And when do symptoms appear? |
1. 25-50% of people 2. Symptoms occur 15-30 yrs after the original infection |
The highest number of Hep. C positive peeps are found among ____________ and _____________. |
Black and Hispanic |
What are some features of fungi? |
1. Affected by Geography & environment ( with damp areas) 2. Associated w/ soil 3. Produce endospores for reproduction 4. Are usually inhaled 5. Recycle organics 6. Opportunistic 7. Major antibiotic producers 6. |
Fungi can be divided into ______________ and _______________. |
Yeast Mold |
Yeasts are typically ____________ and reproduce by ____________. Give an example of one. |
Round/oval Budding
Ex: Candida |
Molds are composed of ____________ that grow _______________ and _____________ extensions. |
Hyphae Branching Longitudinal |
Give an example of a mold. |
Aspergillus |
T/F: Some fungi are dimorphic; both yeast and mold like |
True |
T/F: Candida is part of the normal flora. |
True |
What is responsible for one of the first manifestations of AIDs? |
Candida infections |
What infections can Candida cause? |
1. Thrush 2. Yeast infection 3. Skin and Mucosal infections |
Thrush is characterized by white pustules in the ___________ and _____________. |
Mouth and throat |
Give an example of a dimorphic fungus. |
Histoplasma |
Where does the fungus Histoplasma reside and how is it acquired? |
Resides inside macrophages and neutrophils.
Acquired by inhalation |
Do antibiotics work against fungi? |
No. Use Amphotericin B |
________________ are molds and the causative agent of ringworm. |
Dermatophytes |
If the dermatophytes primarily infects animals it is called ______________, if it affects only humans then it is called _________. |
Zoophilic Antrhopophilic |
Dermatophytosis tend to infect which kinds of sites? |
Scalp Feet Skin Groin |
This dermatophytes primarly affects the groin area and causes Jock itch. |
Tinea Cruris |
Which dermatophyte causes ringworm in legs and trunks? |
Tenia Corporis |
____________ causes ringworm of the scalp. |
Tinea Capatis |
Which dermatophytes causes a fungal infection of the nails. |
Onychomycosis |
Tenia Pedis is seen in young teens and is common in bathing facilities. It affects ____________ and the main symptom is __________. |
Toes Itching |
How does the mold Aspergillus enter the body? |
Inhalation of spores. But can also enter thru traumatized skin |
What are some features of Protozonal infections? |
1. Eukaryotic, unicellular 2. In 2 forms: cysts or trophoziote 3. Classified based on there locomation 4. Fecal-oral route 5. H2O borne also 6. Anaerobic |
Trichomonas vaginalis is a _____________ parasite with no known cyst form. |
Flagellated |
T/F: Men cannot get Trichomanas Vaginalis. |
False; they are also infected |
The cell wall of fungis have _______________ which is a target for anti-fungal drugs. |
Ergosterol |
Which form of a parasite is infectious? which is the growing form? |
Infectious = Cyst form Growing = Trophozoite |
What oral agent is used when scalp and nail infections dont respond to topical therapy? |
Griseofulvin |
What is the significance of Metroniazide in treating anaerobic infections? |
It forms an "electron sink" and inhibits the anerobic respiration and the double helix structure |
Which protozoan infection could be considered an STD? |
Scabies |
What is Scabies? |
Highly contagious parasitic skin infection caused by mites that are host specific to humans and completes its entire life cycle on human skin. |
What are important clinical features of infection by Histoplasmosis? |
1. Severe infections resemble ARDS 2. Causes large pulmonary lesions that become nodules = Histoplasmoma 3. Granuolmatosis and fibrosis that infects lymph nodes 4. If chronic have diseased upper lobes of lung 5. Progressive is usually fatal 6. Can infect choroid 7. African version selectively affects skin, soft tissues and bone not lungs. |
Which body fluids have the lowest amount of Hep. B? |
Urine Feces Sweat Tears Breastmilk |
Which body fluids have moderate amounts of Hep. B? |
Semen Vaginal Saliva |
List some ways to prevent Scabies? |
1. Wash bedding in very hot water (125 F) 2. Avoid sex w/ infected peeps 3. Dry clean clothing 4. Vacuum living room 5. Dont share clothes/towels/bedding 6. Notify school |
Malaria is caused by ______________, and use ________________ as there insect vector to transmit to humans. |
Plasmodium Female Anopheles Mosquitoes |
Which cycle in the mosquito is it when the protozoan turns into the cyst form? |
During the Sporogonic cycle |
Once the cyst form of Malaria bites a human, what cycle does it enter and what organ does it affect? |
Enters the Exo-Erythrocytic Cycle
It affects the liver |
What happens during the trophozoite form of Malaria? |
The protozoan is in the liver. It ruptures and leaves the liver to go to the RBCs. The RBCs can then rupture and regenerate the protozoan. |
During which stage of Malaria infection is responsible for clinical manifestations of the disease? |
Erythrocytic Cycle |
_____________________ is the morphological form which develops in the mosquito salivary gland. It is injected when the mosquito feeds. |
Sporozoite (cyst form) |
What are the typical clinical manifestations of Malaria? |
1. Recurrent high fever 2. Chills 3. Headache 4. Anemia 5. Splenomegaly 6. Weakness |
What can Malarial organism also cause, that will ultimately lead to death? Why does this occur? |
Can cause Splenomegaly. The Red pulp of the spleen is the cemetary for RBC. The spleen enlarges because it has alot of dead RBCs. |
How many new infections of Malaria are there a yr and what is the best means of controlling mosquito pop.? |
600 million/yr Use DDT |
How many deaths per year are associated with Malaria? |
3 million |
Which protozoan invades RBCs? |
Malaria |
Which 2 protozoan infections are associated with HIV infection? |
1. Leishmaniasis 2. Malaria |
Which protozoan infects Reticuloendothelial cells? |
Visceral Leishmaniasis |
Which protozoan is the causative agent for Amoebiasis, and 100,000 deaths/yr? |
Entamoeba Histolytica |
Which protozoan caused flask-shaped lesions in the colon and causes bloody diarrhea? |
Entamoeba Histolytica |
What % of people w/E.Histolytica are asymptomatic? |
85-90% |
How is E.Histolytica transmitted? |
Fecal-ral Sexual |
What are some important features of Giardiasis? |
1. (4pairs of flagella) Flagellated protozoan parasite 2. 1 celled organism 3. Lack ER, Mito, GA and Lyso 4. Protective outer shell 5. Anaerobic 6. Aerotolerant |
Cyst form of Giardia is ingested with contaminated water and food and is passed in ___________. |
Feces |
What animal serves as a reservoir of Giardia? |
Beavers |
________________ causes very distinct, smelly, greasy, frothy diarrhea. |
Giardia Lamblia |
Which protozoan has a very low ID50 and cuases a diarrheal disease? |
Cryptosporidium parvum |
How is Cryptosporidium spread? |
Fecal oral Water/food borne |
What are the 3 types of Cryptosporidiosis that can occur? |
Intestinal Pulmonary tracheal |
How is Leishmaniasis transmitted? |
Via the bite of female sand flies |
Which is the most severe form of Leishmaniasis and is related to HIV? |
Visceral Leishmaniasis (VL) |
There is a _______% mortality rate in VL if untreated and __________% of adult cases are related to HIV. |
100% 25-75% |
What is a possible outcome for G.Lamblia infection? And who is at risk for this disease? |
Found in day cares. Can lead to chornic symdrome of diarrhea that contributes to malabsorption and weight loss. (35-70%) |
Which protozoans are capable of causing skin infections? |
Leishmaniasis and Scabies |
Which protozoan can cause both a skin and systemic infection? |
Leishmaniasis |
What are the signs and symptoms of Leishmaniasis infection? |
1. Persistent fevers, may cycle 2. Night sweats 3. Fatigue 4. Weakness 5. Appetite loss 6. Weight loss |
What are the 3 basic principles of antimicrobial therapy? |
1. Selective toxicity (kill organism not man) 2. Reach the site of infection at inhibitory [M+] 3. Penetrate and bind to target (avoid inactivation and extrusion) |
List the target sites/activities for Antibacterial agents (antibiotics). |
1. Cell wall synthesis (we lack this) 2. Protein synthesis (ribosomes) 3. Nucleic acid synthesis 4. Cell membrane function |
What is murein? |
Means cell wall composed of 2 monomers NAG and NAM that is cross linked. |
Which classes of antibiotics affect the cell wall synthesis? |
1. Clycoserine 2. Glycopeptides 3. Bacitracin 4. Beta lactams |
What is the mechanism of action of Beta Lactam antibiotics? |
Penicillin Binding Proteins (PBPs) are enzymes involved with cross linking bacterial cell wall components. Beta Lactams bind to them and inhibit the enzyme from catalyzing the cross link. |
What are the classes of antibiotics that target protein synthesis mechanism? |
1. Aminoglycosides 2. Tetracyclines 3. Chloramphenicol |
List different Aminoglycosides. |
1. Gentamicin 2. Streptomycin 3. Amikacin 4. Neomycin |
Penicillin is considered to be _________________ because it kills growing bacteria. |
Bacteriostatic |
Why is it harder to achieve selective toxicity with drugs targeting viral diseases and eukaryotic diseases than prokaryotic? |
The cells of viral and eukaryotic diseases are similar to the host. Targeting these cells can accidentally damage the host cells also. |
What is selective toxicity? |
Exploiting differences in structure/metabolism of pathogens and host cells in order to kill the microrganism and not the human host. |
Most antibiotics acting upon the ribosome are ______________, but aminoglycosides are ____________. |
Bacteriostatic Bactericidal |
What are some general properties of Aminoglycosides? |
1. Treatment for severe sepsis 2. Needs O2 for entry into cells 3. Fat insoluble = not absored orally 4. Toxic to kidney and inner ear |
What is the mechanism of action for Tetracyclines? |
Inhibits protein synthesis by preventing amino acyl transfer RNA from entering the A site on the ribosome. |
How does Chloramphenicol inhibit protein synthesis? |
It has a nitrobenzene nucleus that blocks peptidyl transferase blocking the protein synthesis.
(Bacteriostatic) |
What are some drugs that act on inhibiting precursor synthesis of nucleic acids? |
1. Trimtethoprim 2. Sulfonamides |
_______________ is used as a DNA replication inhibitor because it affects _____________, so the bacteria is unable to 'pack' DNA into the cell. |
Quinolones DNA gyrase |
Which antimicrobial agent affects DNA-dependent RNA polymerase, thus blocks mRNA so no nucleic acid is made. |
Rifamycins |
Which drugs affect cell membranes? |
1. Azoles = no synthesis of ergosterol 2. Polyenes (Amp.B) = binds to sterols and causes leakage of components then causes cell death. |
What does Metronidazole do to DNA? |
When it is reduced it can bind to DNA, oxidize it and then cause strand breakage. Works for anerobic infections. |
How can resistance disseminate? |
1. Chromosomally mediated resistance= mutant selection 2. Plasmid mediated resistance = spread of ressitance plasmid 3. Plamid mediated resistance on transposon = spread of resistance gene |
What is plasmid? |
Molecules of DNA which replicate independenly of the bacterial chromosomes. |
What are some ways bacteria can make antibiotics ineffective? |
They can physically and chemically remove the drug.
1. Alter target = lowers affinity for antibacterial 2. Alter the uptake = pump drug out of cell 3. Drug inactivation = enzyemes that kill the antibacterial agent |
How can humans prevent development of antibiotic resistance bacteria? |
1. Dont dispense antibiotics w/out Rx 2. Control misuse of antibiotics 3. Antibiotic policies 4. Surveillance of use coupled w/ monitoring emerging patterns of resistance 5. Control use in industry |
Which organism is responsbile for stomach ulcers? |
H.Pylori |
T/F: H.Pylori and Strep. Mutans are not part of the normal flora. |
False; both are in normal flora |
What are the virulence factors for H.Pylori? |
1. Flagella 2. Adhesins (attaches to stomach lining) 3. Urease enzyme (neutralizes acid so bacteria can grow) |
How do you treat stomach ulcers? |
Lifestyle changes and acid reducers |
What causes plaque and tooth decay? |
Strep. Mutans |
How does Strep. Mutans soften enamel? |
Bacteria can turn sucrose into Glucan (polymer). Glucan allows the formation of biofilm. Biofilm covers bacteria and provides anaerobic growing conditions for bacteria. Fermentation occurs w/ sucrose. This decreases pH Decreased ph softens enamel |
T/F: Strep. Mutans have pilli for attachment. |
True |
List viral infections for which a vaccine is available. |
1. Hep A and B 2. Influenza 3. Measles, Mumps, Rubella (MMR) 4. Polio 5. Rabies 6. Smallpox 7. Varicella-Zoster |