Reading...
Play button
Play button
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;
52 Cards in this Set
- Front
- Back
|
Are Butcher's Warts usually malignant?
|
No
|
|
|
Are common warts caused by HPV usually malignant?
|
No
|
|
|
Are plantar's warts caused by HPV usually malignant?
|
No
|
|
|
Can genital warts be malignant?
|
Yes, but rarely. If they do, they become squamous carcinomas
|
|
|
Describe the nucleic acid of HPV
|
Supercoiled, DS DNA of 8kbp long, w/ 8 ORF's (Open Reading Frames) that code for 8 proteins.
|
|
|
What is the transmission for HPV?
|
Direct contact, fomite, and because it is naked, it can even survive mild chlorine so it can be transmitted in locker rooms and pools.
|
|
|
What are two families in Papovaviridae?
|
Papillomavirinae and Polyomavirinae (which contain vacuolating agents, which are yet to be known to cause disease).
|
|
|
Symptoms of HPV include (not polyomavirus)
|
Warts, sometimes cancerous.
|
|
|
Symptoms of Polyomavirus (not papillomavirus)
|
mainly asymptomatic because the body's immune system can keep it latent, but cannot eliminate it - it is a chronic infection. However, it can be deadly with immunosupression (or pregnant, sometimes, or problems with the reticuloendothelial system), as in the case of polyoma being caused by the JC virus, PML can develop (causes neurologic decomposition, hence problems, including paralysis, dementia, eventually death). JC virus can develop UTI w/normal immunse system. The BK virus can also cause death death w/immunosupression.
|
|
|
What is an example of a vacuolating agent studied? How was it studied?
|
SV40 (Simian Virus 40) found in vero cells, were unintentionally incorported in the first polio vaccine since polio was cultured in vero cells. They do not cause disease in humans.
|
|
|
What is the symmetry of papovaviruses?
|
Icosahedral
|
|
|
How large are papovaviruses?
|
Papilloma are 55nm, and polyoma are 45nm.
|
|
|
Why is it that papilloma (this does not apply to polyoma) cannot be cultured in lab?
|
Papilloma only replicates in proliferating epithelial cells, specifically, at the junctions between basal and columnar epithelia. It is hard to recreate this in lab.
|
|
|
Because papilloma cannot be isolated, what are methods of detection?
|
PCR, basophilic inclusion bodies, and even bovine papillomaviruses
|
|
|
Papilloma are now thought to cause 90% of cervical cancers.
|
True.
|
|
|
Butcher's warts are related to bovine papilloma.
|
FALSE! Their origin is not known.
|
|
|
Bowenoid papules refers to…?
|
Malignant papules caused by HPV.
|
|
|
Is there a good immune response to HPV?
|
Kind of. There may, or may not, be IgG and IgM. Primary, non-specific response is as usual, however. There may be a tendency for certain ppl with certain MHC complexes to be suceptible to consequent carcinoma. Certain MHC may not great affinity to killer cells, thus the CMI allowing for the proliferation of cancerous cells.
|
|
|
Polyomas rarely cause disease. But what are the two types that are oncogenic?
|
JC virus, and BK virus.
|
|
|
How is polyoma different from papilloma?
|
They differ in their site of replication - polyoma can be cultured. They differ in the immune response they trigger: polyoma causes a better immune response, but it is still not big enough to eliminate the disease - it is a chronic, latent infection.
|
|
|
Papovaviruses have two structural proteins that make 72 capsomeres.
|
True.
|
|
|
If a person is vaccinated against Hepatitis B, but is exposed to the virus, what antigen(s) will be present in serum?
|
Only HBsAg will be present. HBcAg will not be present because it is hidden in the core and is only exposed after replication. But even after replication, so few HBcAg is around that vast amount of replication must occur before it is detectable - and this only occurs with chronic states, and since the patient is vaccinated, no chronic state will develop so no HBcAg will be present. No HBeAg will be present either because no replication will take place at all since the body's immune system is ready to prevent that because of vaccination.
|
|
|
Can Hepatitis B be shed while being asymptomatic?
|
Yes, Hepatitis B has great chronicity abilities, and like HIV and Herpes, it can be shed while asymptomatic if the infection is chronic.
|
|
|
Is Hepatitis B is more resistant to drying than other enveloped Hepatitis viruses?
|
Yes.
|
|
|
True/False: Like in all other cases, Hepatitis B infections in children are less severe than in adults.
|
True. If a child develops chronic Hepatitis, it is likely that they will become asymptomatic carriers. An adult, however, is likely to develop extrahepatic disease and chronic active infections that can lead to cirrhosis and hepatocellular carcinoma.
|
|
|
What are the main differences between Hepatitis C and B?
|
For starters, Hepatitis B is a DNA virus, while HCV is an RNA virus. Besides this, Hepatitis B and C are clinically and epidemiologically similar, except that Hepatitis C is more likely to develop into a chronic state (85%, as opposed to HBV's 10%).
|
|
|
Which, of the studied Hepatitis viruses, is the only one that is a provirus?
|
Hepatitis B. It replicates its DNA from an circular RNA intermediate via a DNA Polymerase that acts like Reverse Transcriptase. The fact it can integrate its genome is the cause for the great likelihood for hepatocellular carcinoma.
|
|
|
In Hepatitis B, hepatocellular carcinoma usually develops from the integration of the viral genome. Through what mechanism does Hepatitis C cause cancer?
|
Through cirrhosis; which means that, although HCV is more likely to become chronic and most symptoms are exacerbated than in HBV, HBV is more likely to induce carcinoma than HCV.
|
|
|
Hepatitis A and E are very similar. One difference is in the respectively families they come from. Name these families.
|
Hepatitis A is a picornaviruses, while HEV is a calicivirus (which usually cause upper respiratory infections).
|
|
|
What is the smallest Hepatitis virus?
|
HDV, because it is defective. It is followed by HBV, because it too is incomplete (although not RNA like HDV, but circular like HDV).
|
|
|
True/False: Hepatitis A has three sections to its genome, and only codes for 4 proteins (VP 1-4).
|
True!
|
|
|
Order the Hepatitis Viruses in increasing length of incubation.
|
HAV (2-6wks), HEV (6wks), HDV (3-7wks), HCV (2months), HBV(2-5months). Logic: Enteric viruses spread through fecal-oral so they would benefit from rapid incubation. They are followed by HDV, because its small. It is followed, by HCV, which precedes HBV, which makes sense since HCV is similar to HBV but in an exacerbated form.
|
|
|
Which Hepatitis virus has cubic symmetry?
|
HAV
|
|
|
Hepatitis A is a picornavirus. What other virus that we studied is also picorna?
|
Polio
|
|
|
True/False: Icterus may persist even after virus has been destroyed.
|
True. Icterus is a consequence of leaking hepatic enzymes which make take some time to recover from.
|
|
|
Of the studied Hepatitis viruses, which have prophylactic vaccines?
|
HAV, HBV, HDV - all in one vaccine. Therefore, I can say for sure that these three produce an IgM and IgG immune response. HEV is on it's way. HCV is not here yet - part of the reason is that it does not induce a good humeral immune response - which may be due to it mutating in vivo.
|
|
|
Of the studied Hepatitis viruses, which is most pleomorphic?
|
HBV
|
|
|
Of the studiied Hepatitis viruses, which is for sure of icosahedral symmetry?
|
HBV
|
|
|
Which Hepatitis virus has (-) SS RNA?
|
HDV
|
|
|
Which Hepatitis virus(es) have/has SS (+) RNA?
|
HAV, HEV, HCV
|
|
|
Which Hepatitis viruses are capable of replicating in the cytoplasm?
|
HAV, HEV, HCV, because they have (+) SS RNA.
|
|
|
HAV and HCV are similar in that both are (+) SS RNA viruses, therefore can replicate in the cytoplasm. What other property do they share in protein synthesis?
|
They trasncribe and translate one large protein that gets cleaved into a bunch of smaller functional units. In HAV, for the virions to mature, they have to get cleaved.
|
|
|
What is a possible explanation as to why Hepatitis A is self-limiting.
|
There is cell damage upon release of the virion, enough to prevent it from becoming chronic. However, the majority of the damage to the patient can be attributed to the CMI.
|
|
|
What is the only hepatitis virus that has been cultured in lab?
|
HAV, and even it has been difficult.
|
|
|
HBV has a tendency to become chronic. What is its most likely method of release.
|
Budding. Indeed, that is the method.
|
|
|
Will a patient with chronic persistent HBV have Anti-HBs?
|
No, HBsAg is only present once disease has been resolved.
|
|
|
Will a patient with chronic active or fulminant HBV have Anti-HBe
|
No, because having Anti-Hbe means that some inhibition to replication is occuring, so this cannot be for a fulminant case. However, it is the case for a persistent chronic infection which commonly result in just extrahepatic disease.
|
|
|
Explain the "ground glass" appearance of HBV.
|
Like HAV, HBV is jam-packed with viral antigens so that when it is stained with eosine, it looks like ground glass.
|
|
|
True/False: Orcein stains HBV brown.
|
True.
|
|
|
What is an important epidemiological reason to study HBV?
|
Because in some areas of the world, it is the ldeading cause of hepatocellular carcinoma.
|
|
|
Explain why there exists an HBsAg window in the typical HBV infection.
|
This occurs when enough Anti-HBe has been produced to halt replication and make HBsAg apparently disappear. At is during this window, though, that Anti-HBs (convalescence) starts showing up because of the high Anti-HBe. Eventually, both HBsAg and Anti-HBs are detectable, with Anti-HBs increasing as the infection resolves.
|
|
|
What are some quick detection methods used for HBV?
|
Reverse Passive Hemagluttination. This is when Anti-HBs is introduced into sample serum. If the serum contains HBsAg (the first antigen detectable) then the complex of Anti-HBs w/ HBsAg will aggultinate RBC's. The Latex slide test does the same thing, except its faster.
|
