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HIV, Hepatitis, Herpes. Slackers Facts by Mike Ori. Disclaimer. The information represents my understanding only so errors and omissions are probably rampant. It has not been vetted or reviewed by faculty. The source is our class notes.

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Hiv hepatitis herpes

HIV, Hepatitis, Herpes

Slackers Facts by Mike Ori


Disclaimer
Disclaimer

The information represents my understanding only so errors and omissions are probably rampant. It has not been vetted or reviewed by faculty. The source is our class notes.

The document can mostly be used forward and backward. I tried to mark questionable stuff with (?).

If you want it to look pretty, steal some crayons and go to town.

Finally…

If you’re a gunner, buck up and do your own work.


What are the retrovirus groups


Oncoretrovirus

Lentivirus



Oncoretrovirus – HTLV I/II

Lentivirus – HIV I/II





Onco = tumor

Lenti = slow





HTLV I – Adult T-cell leukemias

HTLV II – Hairy cell leukemias



Reverse transcriptase

Integrase

protease





Structural genes for matrix, capsid, of viral genesnucleocapsid


What is the function of the of viral genespol genes


DNA synthesis and maintenance and protein activation. of viral genes

Protease, reverse transcriptase, integrase


What is the function of the of viral genesenv genes


Surface of viral genesglycoproteins and transmembrane proteins

GP120 and GP41


What does HIV rev do? of viral genes



What does HIV tat do of viral genes




Tax and LTR.rex






What the general mechanisms of with host cell promoters.oncogenesis


Expression of viral genes that interfere with or cause over-expression of host proteins that lead to defective cell cycle maintenance.

Insertional mutagenesis - Insertion of viral genome into the host genome in a way that causes dysregulation.

Acute transforming viruses – incorporate a host oncogene in the viral genome.


What are the primary HIV surface over-expression of host proteins that lead to defective cell cycle maintenance.glycoproteins and what are their functions?


GP120 – interacts with host cell receptors over-expression of host proteins that lead to defective cell cycle maintenance.

GP41 – initiates fusion of viral and host membranes


What are CCR5 and CXCR4 over-expression of host proteins that lead to defective cell cycle maintenance.


These are coreceptor molecules on the surface of some human cells whose binding is required in addition to GP120-->CD4


Where are CCR5 and CXCR-4 found cells whose binding is required in addition to GP120-->CD4


CCR5 is found in dendritic cells and macrophages in the periphery. CXCR-4 is found on CD4 T-lymphocytes


Where is the highest concentration of HIV virus found periphery. CXCR-4 is found on CD4 T-lymphocytes


In lymph nodes periphery. CXCR-4 is found on CD4 T-lymphocytes


Describe why antibodies are less effective against HIV periphery. CXCR-4 is found on CD4 T-lymphocytes


HIV infects adjacent cells during the budding process. It is not exposed to antibodies. Note that HIV proteins on the plasma membrane are targets for antibodies though.


How does HIV reduce its exposure to cytotoxic T-cells is not exposed to antibodies. Note that HIV proteins on the plasma membrane are targets for antibodies though.


It down-regulates MHC-I and MHC-II is not exposed to antibodies. Note that HIV proteins on the plasma membrane are targets for antibodies though.





A, B, C, D, E, G CXCR-4?

Where is F?



A,E – enteric CXCR-4?

B,D – Sex, blood, and rock and roll

C – Blood

G – Enteric?



EBV CXCR-4?

CMV

VZV

Yellow fever


What family does CXCR-4?hep A belong to?




Transmission is ultimately fecal oral CXCR-4?

Person to person

Shellfish

Water



Hepatitis in the late 70’s?has some symptoms we should learn to recognizeLike fever, feeling very tired and loss of appetite.Your stomach hurts, you feel real sick, you will not eat a bite.Your eyes sometimes look yellow when they only should be white.

Wash your hands after going to the bathroomWash your hands after changing baby too'Cause we don't want to spread hepatitisAnd we don't want hepatitis to catch you. Who? YOU!



IgM titer in the late 70’s?



14-40d in the late 70’s?




Why does Enveloped virusHep B have a reverse transcriptase


Hep Enveloped virus B uses RT during the viral replication process to convert whole genome RNA transcripts into DNA.








What is the epidemiology of HBV? a barrier to their efficacy.




10-20% to sexual activity.



Cirrhosis to sexual activity.

Hepatocellular carcinoma (200x increase)



160 days to sexual activity.



Anti core to sexual activity.

Anti surface

Anti E



Anti surface (anti to sexual activity.HBsAg)


Which to sexual activity.Ab is the first to be produced


Anti core to sexual activity.


Which to sexual activity.Ab is next


Anti E to sexual activity.



Anti surface to sexual activity.



The incubation period for HBV is very long. Hence, an early inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


For what other virus is post exposure vaccination used? inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


Rabies virus inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


What is the inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.tx for HBV?


IFN-alpha inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


What family does Hepatitis B virus belong to? inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


Hepadenaviridae inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


What family does hepatitis C belong to inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


Flaviviridae inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


What are the other members of inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.flaviviridae?


Yellow fever, dengue, St Louis, west inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.nile


What is the chronicity for HCV? inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


85% inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


What is the primary mode of transmission of HCV? inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


Needle sharing inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


What are the sequelae to HCV? inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


Cirrhosis inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.

Hepatocellular carcinoma


What is the structure of HCV? inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


Enveloped ssRNA (+) inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


What is unusual about the chronicity of HCV? inoculation can prevent HBV infection from establishing even if the neonate is infected during parturition.


Chronic viruses need to have a method of genome persistence. RNA viruses (HCV=RNA) are generally considered too fragile to persist within cells (replicate or die) but HCV is able to do so through unknown mechanisms.




What is the damage. tx for HCV?


IFN-alpha +/- damage. ribavirin







HDV requires HBV as HDV’s genome does not encode surface antigen. Thus it is impossible to be infected with HDV unless HBV infection is present.


Describe the hepatitis that occurs with HBV/HDV antigen. Thus it is impossible to be infected with HDV unless HBV infection is present.coninfection


Fulminant antigen. Thus it is impossible to be infected with HDV unless HBV infection is present. hepatitis. Often presents as an acute exacerbation in a chronic HBV patient.


What is the diagnostic test for HDV? antigen. Thus it is impossible to be infected with HDV unless HBV infection is present.


Anti-Delta antigen antibody titer antigen. Thus it is impossible to be infected with HDV unless HBV infection is present.


Describe the difference between HAV and HEV antigen. Thus it is impossible to be infected with HDV unless HBV infection is present.


HEV is an unclassified virus similar to antigen. Thus it is impossible to be infected with HDV unless HBV infection is present.calcivirus (ssRNA (+) icosahedral). It is typically only an issue in pregnant women where it can cause fulminanthepititis. Typically found on indian subcontinent.


Why am I not describing Hepatitis G antigen. Thus it is impossible to be infected with HDV unless HBV infection is present.




Please that’s easy… yet linked to disease.

Herpesviridae


What is the morphology of yet linked to disease.herpesvirus



List the herpes viruses yet linked to disease.


HSV-1 yet linked to disease.

HSV-2

Varicella-zoster (VZV)

Cytomegalovirus

Epstein-barr

HHV-6

HHV-7

HHV-8



HSV 1 is above the waist, HSV 2 is below. These are loose rules though as cross infection is known.


What is the tropic tissue for HSV 1/2 rules though as cross infection is known.


Skin where it causes ulcerating lesions rules though as cross infection is known.


Why do people have recurring lesions with HSV 1/2 rules though as cross infection is known.


HSV invades the trigeminal (1) or sacral (2) nerve ganglions. It periodically reactivates and then flows down the axons to replicate in the epithelial cells.


What are the theories for HSV reactivation ganglions. It periodically reactivates and then flows down the axons to replicate in the epithelial cells.


1. Stress and other factors cause the latent virus to begin replicating in the ganglion. The resulting virions are shed from the axon tip and then begin replication in the epithelium. 2. A low level of virus production occurs within ganglion cells and is release in a burst from the axon. These then replicate in the epithelium. (store and release)


What are the gene classes in HSV. What are their functions? replicating in the ganglion. The resulting


Alpha – immediate early, regulatory replicating in the ganglion. The resulting

Beta – early, genome replication

Gamma – Late, structural


What is the role of the LAT1 gene in replicating in the ganglion. The resulting maintianing HSV latency.


LAT1 transcripts are antisense to alpha-0. This blocks the action of alpha-0.

Thus neither can live while the other survives.


Where does HSV assembly occur action of alpha-0.


In the nucleus action of alpha-0.


Where does HSV bud from action of alpha-0.


The nucleus into the ER action of alpha-0.



The inner membrane of the ER. action of alpha-0.



By exocytosis action of alpha-0.



Keratoconjunctivitis action of alpha-0. leading to corneal ulceration



It is a circular action of alpha-0.extrachomasomal element



Acyclovir action of alpha-0.

Foscarnet if resistant



Incubation for 14 days action of alpha-0.

Recovery in 2 weeks


What is shingles action of alpha-0.



Describe the VZV vaccine action of alpha-0.


Live attenuated action of alpha-0.


Describe CMV clinical disease action of alpha-0.


Normally no action of alpha-0.sx except in immunocompromised where it can have sx of pneumonia.

Can cause mono.



Nuclear and cytoplasmic inclusion bodies with owl’s action of alpha-0.eye appearance. Giant cell formation.



Blueberry muffin babies action of alpha-0.

Hearing loss, retardation, hepatosplenomegally



Infectious mononucleosis action of alpha-0.


Distinguish EBV and CMV mono action of alpha-0.


EBV is mono-spot positive action of alpha-0.

CMV is mono-spot negative



EBV elicits action of alpha-0.heterophile antibodies against sheep RBC.



Burkitt’s action of alpha-0. lymphoma in africaand nasopharyngeal carcinoma in asia



Roseola action of alpha-0.infantum

Many other agents cause as well



Kaposi’s sarcoma action of alpha-0.


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