Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
120 Cards in this Set
- Front
- Back
Examples of important oncogenes
|
Ras and Myc
|
|
Three enzymes found in HIV--important targets for antiretroviral drugs
|
Protease, reverse transcriptase, and integrase
|
|
_______ surface protein of HIV interacts with _______ on T-cells
|
GP-120; CD4
|
|
Integrated retroviral DNA has _________ on each end which attract _________ and promote transcription of both viral DNA and normal DNA
|
long terminal repeats; RNA polymerase II
|
|
What is the function of the Myc protein?
|
acts as a transcription factor to activate cell proliferation genes
|
|
What is the cause of most virus-derived oncogenic mutations?
|
Retroviruse integration into host chromosomes which subsequently promotes downstream oncogenic transcription
|
|
Humans Herpe Virus: 1) enveloped/nonenveloped 2)What kind of genome?
|
1) enveloped 2)dsDNA
|
|
Where do most type-1 alphaherspesvirinae establish latency?
|
sensory ganglion
|
|
HSV-2 is associated with:
|
genital herpes
|
|
Cold sores and fever blisters are recurrent infection in:
|
Herpes labialis (HSV-1)
|
|
Ocular infections are associated with
|
HSV-1--the leading cause of blindness in the US
|
|
This drug reduces the transmission of HSV-2:
|
Valacyclovir
|
|
Pregnant women with genital herpes are treated with which drug:
|
Acyclovir
|
|
Anti-HSV drugs are activated by:
|
viral enzymes, predominantly viral thymodine kinase
|
|
T/F: Anti-HSV drugs eliminate the latent virus.
|
False: the latent virus is never eliminated; Anti-HSV drugs are nucleoside analogs that are active only against replicating viruses
|
|
Mechanism of acyclovir:
|
acts as a nucleotide analog; when it's incorporated into the growing chain, it terminates/inhibits DNA polymerase
|
|
Cytomegalovirus: Production infection is seen in ______ and latent infection is seen in ________
|
Cytomegalovirus: Production infection is seen in macrophages and fibroblasts and latent infection is seen in B and T lymphocytes and bone marrow stromal cells
|
|
What are "owl's eyes" cells?
|
The characteristic halo surrounding intranuclear inclusion bodies in cytomagalovirus infected cells
|
|
The most common virus transmitted in utero is ______ and can cause _______
|
Congenital CMV; cytomegalic inclusion disease
|
|
Two best drugs for CMV infections:
|
Ganciclovir and Foscarnet. Note, Acyclovir is not effective at all for CMV
|
|
Compare and contrast Alpha and Beta Herpes Viruses
|
Alpha: very promiscuouse, variable host range, short reproductive cycle, spread rapidly, latent infection stored in sensory ganglion.....Beta: very restrictive host range, long reproductive cycle, latent virus maintained in secretory glands, lypmphoreticular cells, or kidneys
|
|
Most common HHV Type 6 associated disease
|
Roseola, or sixth disease
|
|
What "structure" in the viral DNA is characteristic of all herpes viruses?
|
terminal repeat sequences which encode regulatory genes for the virus
|
|
What is the oncogene associated with Burkitt's lymphoma?
|
C-myc. Burkitt's lymphoma is associated with epstein barr virus.
|
|
Name the drug used to treat EBV:
|
no drugs are available
|
|
EBV is in an alpha, beta, or gamma herpesvirus:
|
gamma
|
|
Which form of Hepatitis does not have a chronic stage?
|
Hepatitis A: antibodies form as symptoms develop
|
|
This form of hepatitis possesses a reverse transcriptase
|
Hepatitis B (HBV)
|
|
Which form of Hepatitis exhibits immune complex disease?
|
HBV
|
|
What happens to HB surface antigen (HBsAg) in acute versus chronic infection?
|
In acute, HBsAg goes up and then down. In chronic, HBsAg remains elevated
|
|
Cellular injury due to HBV is mediated via cytopathic effects of the virus. T/F
|
False. Cellular injury due to HBV is mediated via immune responses
|
|
HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drugs _______ and _______.
|
Ribavirin and Peginterferon
|
|
Which enzyme mediates the transformation of an immature HIV to a mature, infectious virus?
|
a protease
|
|
Does HIV replicate in the blood or lymphatic tissue?
|
lymphatic tissue
|
|
_______ is a marker of the effectiveness of anti-retroviral therapy.
|
viral load
|
|
Active/Inactive CD4 cells can be infected with HIV.
|
ACTIVE
|
|
In the lymph node, B cells reside in the _______, while T cells reside in the _______.
|
B cells reside in the GERMINAL centers, while T cells reside in the PARACORTICAL region.
|
|
What enzyme is necessary to free a new influenza virus from the host cell?
|
neuraminidase
|
|
What influenza viral protein binds to host cell-surface receptors for cell entry?
|
hemagglutinin
|
|
The drug of choice for HSV-1:
|
Penciclovir: a topical nucleoside analog
|
|
2 drugs that treat influenza A only:
|
amantadine and rimantadine
|
|
2 drugs that treat both influenza A and B:
|
zanamavir and oseltamivir/Tamiflu
|
|
MOA for Amantadine and Rimantadine
|
inhibitors of uncoating and thus replication
|
|
MOA for Fomivirsen
|
Inhibitor of translation with antisense mutation
|
|
CMV drugs:
|
Ganciclovir/Valganciclovir, foscarnet, cidofovir, fomivirsen
|
|
MOA for acyclovir and valacyclovir
|
terminates DNA elongation: nucleoside analog- high specificity for HSV and VZV thymidine kinase
|
|
MOA for penciclovir and famciclovir
|
terminates DNA elongation: nucleoside analog- high specificity viral thymidine kinase
|
|
MOA for Ganciclovir and Valganciclovir:
|
inhibits DNA polymerase; activated by cellular and viral enzymes to its active triphosphate form; nucleoside analog
|
|
MOA for Foscarnet
|
Inhibits DNA polymerase
|
|
What ophthalmic drugs are used to treat HSV keratitis?
|
Trifluridine and Idoxuridine
|
|
What two HIV glycoproteins bind to CD4 receptors on the T cell during attachment?
|
gp120 and gp41
|
|
MOA of Maraviroc
|
inhibits interaction between T cell chemokine receptor CCR5 and HIV-1 gp 120
|
|
What is the only HIV entry inhibitor?
|
Maraviroc
|
|
MOA of Enfuvirtide
|
inhibits HIV fusion with cell: binds to HIV gp41 subunit
|
|
MOA of nucleotide reverse transcriptase inhibitors:
|
"False building blocks" that compete with nucleosides and abort DNA synthesis
|
|
MOA of nonnucleotide reverse transcriptase inhibitors:
|
bind to the reverse transcriptase, causing disruption of the enzyme's catalytic site; Ex. nevirapine- the drug given to pregnant women
|
|
MOA of Raltegravir
|
inhibits HIV integrase which covalently links the viral DNA to the host genome
|
|
MOA of protease inhibitors
|
prevent cleavage of the polyproteins into smaller proteins which are able to infect new cells
|
|
What class of HIV drugs are potent inhibitors of the CYP450 system?
|
protease inhibitors
|
|
Name common side effects of protease inhibitors:
|
dorsocervical fat pad ("buffalo hump"); peripheral lipodystrophy syndrome (fat redistribution)
|
|
the virus of the common cold
|
rhinovirus
|
|
this enterovirus can spread to the heart
|
coxsackievirus
|
|
this enterovirus can spread to the motor neurons in the CNS
|
Polio virus. The secondary infection is called poliomyelitis
|
|
Which has the broadest range of infection: rhinovirus, polio virus, or coxsackievirus? Why?
|
Cosackievirus, because its host receptors are broadly distributed across the body
|
|
MOA of polio vaccine
|
contains all 3 polio virus serotypes and prevents poliomyelitis by neutralizing viremic polio (thus, doesn't prevent primary polio infection)
|
|
Regarding polio, the ______ vaccine utilizes a killed virus while the _______ vaccine utilizes a live, attenuated virus.
|
The SALK vaccine utilizes a killed virus while the SABIN vaccine utilizes a live, attenuated virus.
|
|
The Rhinovirus receptor molecule is ______ and is found predominantly in _______ tissue.
|
The Rhinovirus receptor molecule is ICAM-1 and is found predominantly in NASAL tissue.
|
|
T/F: There are no vaccines against rhinovirus.
|
True: Rhinovirus undergoes extensive antigenic variation (as does HIV) and makes the development of a vaccine impossible. Rhinovirus has more than 100 serotypes.
|
|
In cases of Respiratory Synctial Virus and Measles, synctia are detected in the histology. What are synctia?
|
Multinucleated giant cells that form because viral fusion protein is produced and appears on the surface of infected cells, fusing the cells together.
|
|
The predominant viral cause of acute lower respiratory infection in childhood and most common overall cause of bronchiolitis:
|
Respiratory Synctial Virus: child presents with history of funny nose, followed by cough and rapid breathing, chest retractions, low grade fever, and wheezing on auscultation
|
|
______ is the typical manifestation of parainfluenza virus.
|
CROUP--narrowed, inflamed trachea due to edema and swelling
|
|
_______ have non-segmented RNA genomes while _______ have segmented RNA genomes. Segmented genomes allow antigenic SHIFT through genome reassortment.
|
PARAMYXOVIRUSES have non-segmented RNA genomes while ORTHOMYXOVIRUSES have segmented RNA genomes. Segmented genomes allow antigenic SHIFT through genome reassortment.
|
|
"CCC and P"- cough, coryza (runny nose), conjunctivitis, photophobia; Koplik's spots....these are manifestations of ______.
|
Measles
|
|
_____ is unlike other paramyxoviruses, in that it has no fever, rash, or pneumonia, just parotitis.
|
Mumps
|
|
All ________ viruses are enveloped.
|
negative strand RNA
|
|
During the _______ phase, the virus has been uncoated and has released the genome, but has not yet replicated.
|
eclipsed phase
|
|
________ shields the virus from the immune response.
|
Glycosylation
|
|
___ strand RNA viruses encode RNA polymerase, but do not carry it in the virus, while ___ strand RNA viruses actually carry the RNA polymerase in the virus.
|
+ strand RNA viruses encode RNA polymerase, but do not carry it in the virus, while - strand RNA viruses actually carry the RNA polymerase in the virus.
|
|
New viral strains are formed via ________.
|
segmented genomes
|
|
The best predictor of HIV outcome is ________.
|
the viral load
|
|
Do skin lesions in small pox reflect primary or secondary viremia?
|
secondary
|
|
Burkit's lymphoma is associated with what virus?
|
Epstein Barr Virus
|
|
What cytokines induce an antiviral state in the cell?
|
Type 1 interferons; interferons alpha and beta
|
|
the presence of dsRNA in a cell will trigger the release of _______.
|
type 1 interferons
|
|
Type I interferon inhibits cellular protein synthesis by activating two pathways, ____________ and ____________.
|
Type I interferon inhibits cellular protein synthesis by activating two pathways, 2'5' oligoadenylate synthase pathway which degrades mRNA, and the Protein Kinase R pathway, which inhibits translation.
|
|
Viral nucleic acids are inside this viral structure:
|
icosahedral virus
|
|
Viral nucleic acids are integrated with viral protein, forming the structure of the virus. This describes a ____________.
|
nucleocapsid
|
|
The influenza antigen, _______, interacts with _______ on the surface of the target cell.
|
The influenza antigen, HEMAGGLUTININ, interacts with SIALIC ACID on the surface of the target cell.
|
|
What are the molecular signals for viral protease to cleave out the individual viral proteins from a polyprotein?
|
Gln-Gly pairs
|
|
Multiple proteins encoded on one mRNA describes a ________.
|
Polyprotein
|
|
In ___ strand RNA virus, the strand must be transcribed first before protein translation.
|
negative strand RNA must be transcribed to a positive strand which is then translated.
|
|
How do non-retroviral DNA viruses cause tumors?
|
by encoding proteins that inhibit tumor suppressor pathways, such as the Rb protein
|
|
In HHV, tegument proteins are responsible for ________.
|
promoting viral transcription following infection
|
|
If viral DNA is maintained in EPISOMAL form, then the viral DNA has not been ________ and the virus is in the ________ stage.
|
If viral DNA is maintained in EPISOMAL form, then the viral DNA has not been INTEGRATED and the virus is in the LATENT stage.
|
|
Do cytomegalovirus disease symptoms occur in primary or recurrent infections?
|
Primary: the clinical syndrome is mononucleosis
|
|
Gamma Herpesvirus replicate in ________.
|
Gamma Herpesvirus replicate in LYMPHOID BLASTOID CELLS and can transform B-cells into immortalized lymphoblast-like cells.
|
|
EBV are tropic for cells that have the same receptor for the ______________.
|
EBV are tropic for cells that have the same receptor for the C3d COMPONENT OF THE COMPLEMENT SYSTEM.
|
|
This acute disease can cause a massive loss of hepatocytes in 2-3 weeks that results in inflammatory infiltrates, an exaggerated immune response, and can sometimes cause a shrunken liver, a wrinkled capsule, or a collapsed reticulin network.
|
Fulminant hepatitis
|
|
Fulminant hepatic failure is most common in _________.
|
HBV
|
|
What form of hepatitis causes liver fatty change?
|
HCV
|
|
_________ can reduce mother-to-child HIV transmission, but HIV will become resistant if the drug is used alone.
|
Navaropine
|
|
What is "Ritonavir-boosting?"
|
Ritonavir, a protease inhibitor, inhibits the CYP450 system, allowing other drugs to be more potent
|
|
Of the following paramyxoviruses, which cause viremia? Measles, Parainfluenza, Mumps.
|
Measles and mumps cause viremia. Parainfluenza does NOT.
|
|
This influenza protein cleaves sialic acid and prevents virion clumping
|
Neuraminidase
|
|
Two neuraminidase inhibitors, _______ and _________, work against influenza by ____________.
|
Two neuraminidase inhibitors, ZANAMIVIR and OSELTAMIVIR, work against influenza by INTERFERING WITH VIRION RELEASE AT THE CELL SURFACE.
|
|
Is the injected influenza vaccine a killed virus or live, attenuated virus?
|
killed
|
|
T/F: There have been no human-human transmission of avian H5N1 influenza strains.
|
True. Only human-human transmission can cause a pandemic. So far, there has only been avian-human transmission of the avain H5N1 strain.
|
|
non-enveloped, linear double-strand DNA respiratory virus
|
adenovirus
|
|
this virus is non-seasonal, seen mostly in young children, and only has human-human transmission.
|
adenovirus
|
|
Adenovirus infections typically occur in the _____.
|
lung, GI, and eye
|
|
What virus can hemagglutinate RBCs?
|
adenovirus
|
|
Adenovirus DNA replication, DNA transcription of mRNA, and virion assembly all occur in the host cell _______.
|
nucleus
|
|
What virus is used as a gene therapy vector?
|
adenovirus
|
|
Fever, headache, altered mental status, and focal neurologic signs indicate __________, while fever, headache, neck stiffness, and normal mental status indicate ____________.
|
Fever, headache, altered mental status, and focal neurologic signs indicate VIRAL ENCEPHALITIS, while fever, headache, neck stiffness, and normal mental status indicate BACTERIAL MENINGITIS.
|
|
Cytokine activation resulting in vascular collapse, internal bleeding, thrombocytopenia, and increased hematocrit
|
Dengue Hemorrhagic Fever/Shock Syndrome: caused by a vector borne virus
|
|
Bradycardia with fever is called _________ and is associated with ________.
|
Bradycardia with fever is called FAGET SIGN and is associated with YELLOW FEVER.
|
|
cause of cervical cancer
|
HPV-18
|
|
HPV proteins: ___ complex ubiquinates p53 and promotes its degradation. ___ promotes the degradation of Rb protein.
|
HPV proteins: E6 complex ubiquinates p53 and promotes its degradation. E7 promotes the degradation of Rb protein.
|
|
Alpha HPV has tropism for _________, may cause ______ warts, and include the viral strains that cause _________.
|
Alpha HPV has tropism for GENITAL-MUCOSAL SITES, may cause GENITAL warts, and include the viral strains that cause CERVICAL CANCER. (HPV-16,18)
|
|
Common, cutaneous warts are caused by ___ HPV.
|
beta HPV
|