DIP Episode 2 - (Viral Cases A)

Okay, welcome. My name is a divine. Here is our second podcast. And today we're largely going to talk about viruses. And before I go into that, I just like to wish ever woman out there a happy woman's day. You certainly put up with a lot of crap on a daily basis. And we appreciate your work, your efforts and the wonderful things you do for humanity. Okay, so let's go ahead and begin. So HIV patient and just real quick, this is going to probably be in like three parts. The ultimate goal is to cover all the material relating to viruses that's tested on the USML step one. So this podcast will just basically go into some detail on like a third of the material. Okay, we're basically talking about the big girl viruses today like the HIV, the HSV, the Herpes viruses and all that one stuff. Okay, so let's start. Now the first question says, HIV patient presents with disseminated, raised skin lesions with central ombillication. Right? So raised skin lesion, central ombillication. Hopefully you're thinking of moloscom contegioso. Okay, moloscom contegioso. And remember that it is it is in fact a kind of box virus. And the way this is spread is basically by direct contact. So if you have contact with lesions, you're getting to trouble. And while we're on the subject of box viruses, again, one of the annoying things that step one will want you to know is that the box viruses, they have their own envelope.

And they're replicating the cytosol, which is kind of different from other viruses. They do replicating the cytosol. So they actually come with their own RNA polymerases. Okay, they come with the own RNA polymerases and they won't make their own surrounding envelope. Okay, so those are just high of things to know. Now, remember that of your box viruses, you also have like cowpox. That's the thing that's classically known as the milk made blisters is sort of presents very similar, similarly to, to virus cellar, which is a kind of herpes virus, but in virus cellar, the lesions are in different stages of healing. In cowpox, the lesions are typically like in the same stage of healing. So just something there to sort of help yourself out. Okay, and then remember that there's such a thin as chicken pox chicken pox is a vaccine preventable. Okay, you get the vaccine, you don't get the bug. Okay, so let's see. So the second one. So a patient on that is you map presents with a three week history of quadriplegia. MRI is notable for an increased preponderance of white metal lesions. So another lesio map is a drug you've probably heard of, right? It's a drug that's used to treat multiple sclerosis. It's an inhibitor of alpha-4 integraine. So when you inhibit alpha-4 integraine, the inflammatory cells that mediate a lot of the damage in MS do not go through endothelial cell barriers and they don't cause any havoc in the central nervous system.

Okay, so if they describe a person, I mean people with MS have neurologic deficits, but if you notice the rapidly progressive nature of these neurologic deficits and you're not talking about viruses, I am really hoping you're thinking about the JC virus and progressive multifocal look and cephalopathy. Okay, so it presents as massive demyelination in the central nervous system and it can cause like a very rapidly progressive set of neurologic issues. Okay, and the classic populations affect that one population of HIV patients that have very low CD4 accounts, usually it's less than 50 and it also affects people that are taken on an lesio map, okay, for for multiple sclerosis. You can also see a retoxymab association, but it's primarily not a lesio map on HIV patients that are tested on the boards. Okay, now next question says hemorrhagicist stitis in a patient who recently got a kidney transplant. This is also a relief head virus because the thing is the JC virus is actually a polio virus. The BK virus is also polio virus and the BK virus, the classic presentation is a person that had a kidney transplant presents with a red urine. You want to think about hemorrhagicist stitis and think of that being secondary to the BK virus. Okay, that's literally all you need to know about that bug. And so I don't forget the polio virus, it's you definitely want to know that there are non-unvelope viruses.

Okay, they're double stranded DNA viruses, they have a circular genome and they're icosahedron. Okay, I know it's kind of annoying, but step one classically, push these questions where they tell you everything and the question you're like, oh, I know the bug, I know the answer. And then you read the answers, you're like, man, are you kidding? And the answer judges have like circular, helical, negative, single stranded blah, blah, blah, blah, blah. Okay, so these little details, they're very good for flashcard material. There are things you definitely want to know. And then at the bottom of the slide, I mentioned all the high-yield causes of hemorrhagicist stitis. So two bugs on one drug. So in addition to the BK virus, remember that at no virus, the classic cause of pink eye. So the buzzword there is faringo conjunctivitis. Okay, causes a hemorrhagicist stitis. And then also remember that she's to sum a hematobium, right? So you've these mentioning everything about Egypt in an exam question or some guy swimming in the mouth. And then the guy has a ready to rent. You want to think about a hemorrhagicist stitis from a hemorrhagicist stitis. Okay, and remember that she's to sum a hematobium. You get that through like direct skin penetration. Okay, and then the one big drug. I hope you're thinking of the alkalinity in agent cyclophosphamide. Remember one of its metabolites known as acrolym. Okay, it's very toxic toxic to the bladder.

Okay, and you can prevent that by giving a mesna. Okay, mesna can bind up that nasty acrolynam breakdown product of cyclophosphamide. You could also potentially give a nacidol system. It also sort of works for that purpose as well. Okay, next question. So pet store owner is rushed to the hospital by ambulance. With a 24-hour history of bloody diarrhea and vomiting. Physical exam is notable for hemorrhagic, ocular and oral effusions. Here it turns from a one-week trip to Nigeria where he performed studies on rats. Ding, ding, ding. So if you see a person that is having hemorrhage from like every notable orifice in the body and you see a rat history, a history of rat exposure, you really want to think about lasa fever. See, lasa fever. Okay, lasa fever, it's a kind of arena virus. It's a single stranded arena virus with lasa fever, rat exposure. And while we're on the topic of rats, if they describe, but remember that leptospirosis, right? So it's a spirochete, leptospirin, terrogens. It classically causes like ocular lesions as well. And they always mention like some history of like visiting Hawaii or swimming in like somebody of water that has like rat urine or some other kind of rooting urine. Okay, so that's another rat association to sort of keep in mind. Okay, and lasa fever is caused by the lasa virus. You can treat it with ribo-viring, but that's like mega mega luio.

It's probably noio for the exam, but I guess if it showed up out of the blue, you'll be thankful you knew the answer. Okay, so next slide. So 17-year-old female who went spalonkin three months ago. Oops, sorry, let me correct that. One of the benefits of having Google Drive. So 17-year-old female who went spalonkin three months ago is comatose in the ICU. She was initially brought to the hospital by concern family members when she did not be or eat or drink for a two week period. So what's the diagnosis, right? So I sort of wrote this question to kind of throw people off and I guess force you to think a little harder than normal. Okay, because if you see spalonkin like, whoa, histoplasmic capsulatum, but histoplasmosis does not make you comatose and it does not make you not want to eat or drink or bathe. Okay, um, so I guess while I'm on this, I'll just go ahead and talk about this testicin strategy. If information is not given in accused them, okay, do not try to make up information that will make an answer that you're really eyeing. Sound really good. Okay, I didn't say anything about a pulmonary infection or cough or anything like that. So don't assume that information to be true, okay? So on an exam, they'll potentially put histo as an answer choice. Do not pick that answer choice. Okay, now, so this person, if you go spalonkin, right, let's assume you potentially were exposed to a bat or a scunk, okay? And then you'll begin to have all these problems, right?

So you don't want to be because you're trying to avoid water. Um, you don't want to eat or drink because you have like spasm of your firing geomossules or you're sort of like trying to like, oh, not taking any kind of water. With all these clues of giving you, what are you thinking about? I hope you're thinking about them, rebbees. Okay, remember rebbees has the bad association, a scunk association or a cool association. Dogs could also transmit rebbees, but that's classically not in the US. That's more in like foreign countries because in the US, dogs get very good vaccinations. Okay, so this is, this is rebbees. Okay, and remember on histology, you'd potentially see something known as a negribody. Okay, a negribody on histology is like an eucinophilic, uh, I believe it's a cytoplasmic inclusion that you tend to find in some cells in the brain like CNS rebbees, like in perkingi cells or pyramidal cells or things like that. Okay, and the cell biology time here is that rebbees, the thing it does is it initially affects, in fact, like um, um, skeletal muscle cells. Okay, you can also, I guess you can also infect neurons initially, but it usually infects the skeletal muscle cells and then it finds its way, uh, so it usually gets in through like a nicotinic acetylcholine receptor and then it finds its way and then begins to infect, um, neurons.

Okay, and it then goes in retrograde transport with, uh, in neurons all the way back to the CNS and then when it gets to the CNS, your screw pretty much, okay, and the thing is, the cell biology time I'm trying to talk about here is, um, step one could make an unusual question where they talk about antigrade versus retrograde transport, okay. Remember, um, antigree transport is meditated by kinesens, okay. Uh, that's a kind of motor protein and then retrograde transport, which is what, um, the rebbees virus uses will be meditated more by dynines, okay, the dynine motor protein. So that's just something to sort of keep in mind. Now, if they ask about the next step in management, after a person has been potentially exposed to, uh, rebbees virus infection, you definitely want to think about giving the person the vaccine, okay, but you also want to give the person rebbees an immune globular because once rebbees gets to the CNS, um, that is pretty much the end. You definitely do not want to be, uh, be under those conditions, okay. And rebbees causes like forming at the mouth, so like a lot of hypersalization, um, and it's just from a dysregulation of the autonomic nervous system. Uh, the psychiatric med that's associated with hypersalization is also the side, uh, one of the psych meds that have been shown to improve survival. And, um, I guess in psych, if you say improve survival, it means prevent, reduce the risk of suicide.

Um, it's an it-y-tipic狀態 psychotic, which is a clasope, okay. Remember the association with a granulose itosis with that. Now, the next slide, a three-year old male from San Francisco, um, has a light base and amylase elevations at five times the oprylimin of normal, right? So hopefully you're thinking of pancreatitis with that, has big testicles, okay. Big parodids and low-grade fevers, okay. So what do you think? It's a vaccine preventable illness that's the hymns I'll give you. So this is moms, okay. So this is the mom's virus. Remember it causes a paratitis, also causes an orcitis, okay. And you could prevent this by getting the vaccine, okay. Um, don't be an anti-vaxer. Never does good for anyone, okay. And if you get a question, so why were on the topic of big testicles if you may? If you get a question about a boy with enlarged testicles, at a long face, at large ears, and more treatment or retardition, I'm hoping you're thinking of fragile like syndrome, okay. It's one of those training, triothide-repeat disorders, but unlike most of the others, it's not a rozomo-dominant inheritance, it's actually ex-linked inheritance, okay. So in general, or girl does not have fragile ex-syndrome on USMLE exams, it's boys, okay. And the pathophysiology is from having CGG repeats, okay. So you have a relatively unstable ex-chromosome, okay. So CGG repeats ex-linked inheritance and classic issues of invoice, okay. Now next slide. The discussion of the Herpes viruses, okay.

So the Herpes viruses, Herpes is super, super high-youtu, not about for your exam. So let's say some things about Herpes. First, I'll talk about some general characteristics, right. So clearly, Herpes is a DNA virus, right. It's a double-stranded DNA virus. I will say that probably the only high-yout single-stranded DNA virus you need to know for step one is parable B19, right. Which causes an aplastic crisis in a sickle cell patients, okay. So the Herpes viruses, the double-stranded DNA viruses, we have an icosahedral capsid, most DNA viruses, not always for both. Most of them do, in fact, have an icosahedral capsid, okay. It's an envelope virus, okay. And it's very, it's like mega high-youtu, no. That Herpes gets its envelope from the nuclear membrane, okay, from the nuclear membrane. That's why, again, if you do a Zank smear, you see an intra-nuclear inclusion, okay, because it's assembled in the nucleus, okay. You may occasionally see like more tiny nuclear giant cells also in the Zank smear. And again, the reasoning behind that is many DNA viruses, of which the Herpes virus is a part, they have something called a fusion protein. And a fusion protein is just basically what they used to attach one cell to the other to begin to move from cell to cell, cell to cell, okay. So when you have that movement from cell to cell, you have all those cells fused together, you form the multi-nuclear giant cell, okay. It's a kind of a sensation.

Now, so let's just sort of go down the Herpes viruses one by one, okay. So human Herpes virus one, okay. And human Herpes virus two, right. So that's HSV one and two, okay. So for HSV one, the classic description is you'll find lesions above the waist, okay, versus HSV two where you find lesions below the waist. That's not always true, but it's a rough approximation, okay. So what are the high yield things you want to know about these bugs, okay, especially HSV one. For HSV one, it can cause a kind of conjunctivitis, okay. In fact, if you see the buzzword, the endritic ulcers on fondoscopic exam, classically in an immunocompromised patient, think about HSV conjunctivitis, okay. And remember that HSV one can cause an encephalitis, classically of the temporal lobes, okay. So if you see like like lesions on MRI in the temporal lobes and a person is like some on the length and they have like an altered mental status, you want to think about HSV temporal lobes and sephalitis, okay. And then if a person has many anxieties with herpes, the classic finding, this is very classic on NV Me exams. If you see a person that has, you do a lumber puncture, you see the CSF, you see like a ton of red cells, you can practically stop reading the question and go ahead and pick herpes, okay. That is the classic way it's presented on these NV Me exams, okay. And how would you treat herpes infection, right.

You'd give a cyclover, I mean if you have like meningitis, you'd probably go ahead and give IV cyclover. Remember the association with nephrolithiasis with a cyclover, but it's a relatively clean drug. And remember that for a cyclover to work, right, it needs to be activated by a thymidine kinase that is expressed solely by the herpes virus, okay. So that's why it does not classically cause like bone marrow problems in humans. And contrast that with CMV, the CMV treatment, GAN cyclover, it's not activated by a thymidine kinase, it's activated by a UL97 kinase, okay. So if you obviously have mutations in these kinases, you have resistance to these drugs. And then if you have like acyclover resistant herpes, you can go ahead and give a false carnage. Remember, it's a pyrophospheda, pyrophospheda analogue, okay. And then HSV2, like I said, classically it's below the waist, causes like pin-pin-four vesicles on an erythemyrus base. And it actually leaves dominant in the sickle ganglia. Contrast that with HSV1, that leaves dominant in the trigeminal ganglia, okay, in the trigeminal ganglia. Okay, and how do you diagnose herpes? Most people go ahead and go PCR at this point, but you may still see the Zank smear business on the USMLE. The Zank smear basically helps you detect HHV1, 2, and 3, okay. So you really cannot tell the herpes' simplex virus apart from the VZV virus on a Zank smear, okay. That's why again, most people go ahead and just do the PCR. Okay, so moving on.

So herpes 3, that's a VZV, okay. You'll get this through like respiratory droplets. I mean, you can also get it by direct contact, but think about it. If you see like the shingles lesion or the VZV lesion of person's skin, you're probably not gonna touch it, right? You're, you won't like know you say, oh, let me just smother these lesions on your skin. No, you don't do that, so you don't get infected. So the respiratory route is the primary route of transmission of the VZV virus. And these methods of transmission believe it or not, are very high out for the test. So classic description, right. Vesicles in different stages of development are contrasted out with the smallpox virus we talked about where you have lesions in the same stage, okay. In VZV, you'll classically see like the motor distribution of lesions in different stages of healing, okay. And it tends to lay dominant in the dose or anglia, okay. In some people, it also lays dominant, especially for like ocular VZV or for like VZV on the face, lays dominant in the trigeminal danglia, okay. And it can reactivate as shingles later in life. So classically, that's in a dermatoma, dermatoma distribution. And that's why you want to get the shingles vaccine, at least a booster vaccine when you hit the age of 60, okay. And again, you can treat VZV like acyclover, if it's resistant, you can give the classic force connect.

And if they give you an example, question about a person that got the VZV vaccine, especially a kit, okay. And then they have like very low blood glucose levels and they have like, they're like comatose. Now you want to think about rice syndrome with the administration of aspirin. Remember, the only kids that should get aspirin, kids that have Kawasaki's disease, okay. Not kids that have like a viral infection, like a febrile viral infection. If you give them aspirin, although it's like super, super rare, but there's a very strong association with aspirin administration and the rice syndrome with kids that have like febrile viral illnesses, okay. Now, VZV is in fact vaccine preventable, okay. It's a life at a new-thed virus vaccine. So for person is severely immunocompromised or a kid that's less than one year old or pregnant woman, you probably do not want to give them the VZV vaccine, okay. But if a mom has been exposed to VZV or neonate has been exposed to VZV, the treatment in that instance is to give the varicela-sostraimium globulite, okay. So VZV, okay. You do not give the vaccine, you give VZV, okay. Now, let's go on to her piece four. So that is EBV, okay. So remember the B in EBV as telling you the cell that is classically infected by EBV, okay. So EBV infects B cells, okay. And it's also, and it actually gets in through the CD21 receptor, okay. It's one of those high-o things you want to know. And it actually also stays latent in B cells, okay.

So sort of think about this. If EBV stays latent in B cells, that should sort of explain why EBV causes many D cell problems, okay. So for example, it can cause a Burkett's lymphoma, okay. Remember the association with an 814 translocation and the starry sky appearance on histology, okay. It could also cause a CNS lymphoma, okay. Classically, that's like a single ring enhancing lesion on MRI, in a patient with a history of HIV, okay, or like severe AIDS, okay. And the thing is these B cells, your immune system is like, man, let me go and deal with these B cells and sort of knock them out. It sends T cells to the rescue. And those T cells, you can actually see them in a blood smear. Those are the cells that are known as the Downy Cells that are classically associated with EBV, okay. And EBV, just another concertine here, loves to infect Nizofarangilla epithelial cells, okay. So it does in fact have an association with a Nizofarangilla carcinoma, okay. And how do you diagnose EBV? You do the monospot test, okay. It's classically monospot positive if you see like, monospot negative mononucleosis syndrome, you're probably thinking more along the lines of CMV, okay. And again, the way EBV will present is youngish person, okay. Let's assume they potentially kissed someone recently. And then they present with Farrangitis, the sort of looks like strep pneumo, I mean, sorry, like strep hyogenes, but they are differences, right. So first things first is the age range, right.

Like, let's assume little kids do not kiss other people, okay. Let's assume it's the, you know, the most sexually active young person that's kissing other people, okay. So, so a youngish person like a teenager, okay. Presenting with Farrangitis, they have more posterior cervical infadenopathy, contrast that with the anterior cervical infadenopathy, you get with strep hyogenes, okay. And they also like feel like super fatigue, like white thalte and they have like splenomegaly, okay. That's why they are classically told to avoid our contact sports, okay. So if you see all those things, get the monospot test, if it's positive, you're thinking EBV, okay. And remember that EBV causes some, besides the CNS lymphoma eight patients, it also causes something known as an oral hairy lucoplicia, okay. So basically, it's like you see like hairy like projections from the tongue and it's not scrappable on like the lesions you find with a candida and a oral throsh. Okay, so let's go to her piece five, okay. This is CMV, okay. CMV you can transmitting in many ways, right. So by getting blood, by getting a transplant, that's a classic association of an exams from sexual transmission, you can also get that. And this is classically monospot negative on like EBV that's monospot positive, okay. And it doesn't stay latent in some weird ganglion, it actually stays latent in mononuclear cells, okay. Stays latent in mononuclear cells.

And the classic description of the lesions you see on histology, intra-nuclear, outside inclusions, okay. So you definitely want to know that for CMV, it is in fact the most common congenital infection in the US. The weight presents, it presents as like a blueberry muffin rash. And this kid almost always has at least an exam, not only in the real world, but an exam has like sensorineural hearing loss, they'll have like jaundice, they'll have like big spleen, big liver, so a pardosplinomagaly, and they tend to have calcifications in the brain. So here's the thing, remember that toxoplasmosis can present as a blueberry muffin rash, just the same way that CMV presents as a blueberry muffin rash. And toxoplasmosis can also present as calcifications in the brain, just the same way that CMV presents with calcifications in the brain. But the big thing and we almost always have to put this on exams to get you to pick the right answer, is the calcification distribution in CMV, it's periventricular, okay. If you see periventricular calcifications on like brain imaging of a neonate, stop breathing the question and pick congenital CMV, okay, versus the intracranial calcification. So you find calcifications like in the cortex and all over in toxoplasmosis, okay. And some other associations for CMV, right. So in transplant patients or AIDS patients, it tends to cause like a red nitase, you can cause like a severe inflammation of the colon, so colitis.

You can also get esophagitis with CMV actually, okay. Remember the CMV esophagitis has the linear ulcers, contrasted out with HSV esophagitis that has the ponch thalta ulcers in the esophagitis, okay. And you treat CMV with GANSI clover, okay. Remember that's activated by the ul 97 chymix, okay. So that's also the mechanism of resistance. And if that's resistant, you can go ahead and give force carnate, okay. And GANSI clover, the high outside effect you want to noise the bone marrow suppression with that, okay. Now, herpes six causes something called exanthensubitum, okay. And like the way it sort of rolls off the tongue, that's the rozilovirus, okay. This is again transmitted via respiratory droplets, okay. And the, practically the only thing you need to know about this is the described child that has super high fever, like 105106. And then boom, the fever is resolved. And then like two, three days later, you see this rash that shows up classically on the cheeks. If you see that, you really want to think about the rozilovirus, okay. Herpes six, okay. Now herpes eight, the big thing you want to know is this is the carpocystochoma herpes virus, okay. Classically, it affects eight species. Okay. So you see like the purplish lesions on the skin, okay. It's an angioproliferative malignancy, if you may. And the mechanism behind that is that HHV eight does, in fact, express a gene that activates a vascula endothelial growth factor, okay.

That's why it's like an angioproliferative malignancy. And one thing they will try to trip you up with on step one is distinguishing carpocystochoma from bacillary angiomatosis, okay. Because the presentation is extremely similar, okay. So the thing is, in bacillary angiomatosis, though sometimes give you a history of exposure to cats, okay. Because remember, it's known as the cat scratch disease and it's transmitted by Bartonella Hensley, okay. Another thing they could say is, oh, they did a biopsy of the skin lesions and you saw a ton of lymphocytes. If you see a ton of lymphocytes, that is carpocystochoma. If you see a ton of neutrophilps, that is bacillary angiomatosis, okay, from Bartonella Hensley, okay. Remember the Worthing Starry Sky, I mean, sorry, Worthing Starry Stain that's used for for Bartonella, okay. So that's all I'm going to say about the herpes viruses. Hopefully you find that useful and I know this is kind of going along. So we're going to try to finish up relatively quickly. Next question says, a 12 month old child with whiz in. There's no family history of asthma or a topic. The child had a sore throat and ran a rare for the past week, right. So you'll see like a viral like presentation and the kid has whiz in. So you're thinking more of a lower respiratory tract infection. Hopefully you know this is RSV, the respiratory sensation virus, okay. RSV, it's the respiratory sensation virus.

It's a paramix of virus, so it's a single stranded RNA virus and it's enveloped, okay. It's an enveloped virus. Now, if you hear whiz in in the kid that is less than two years old or classically less than 12 months old, you should have a very good reason for not picking RSV, okay. And the way you treat RSV, it's really controversial, but you could potentially give ribo-virin. It works in some people, doesn't work in others, okay. And you could prevent RSV, especially in a kid that has like a very high risk of recurrent like respiratory infections. So let's say they have like a touch in a syndrome or they have like cystic fibrosis. You'd want to profile acts against that by giving a monoclonal against the RSV virus, okay. In this case, there'll be a Palavizio map. And if you see a kid that is less than five to six years old on an MBME with a strider, so strider is more indicative of an upper respiratory tract infection. The things you sort of kind of want to think about are either superglotic infection, so epiglotitis, classically caused by H-fluty B, or subglotic infection with the pyrin-flensovirus, which is CROPE, okay. Classically CROPE, you see the wine bottle sign or you could see the steeple sign on a neck x-ray, okay. So those are things you want to think about with that. Now, the last two slides basically talk about HIV, right. So in this slide, hopefully you see my writing, I talk about the life cycle of HIV and soda introduced the pharmacology, okay.

So basically, HIV binds to CD4 with GP120, okay. Remember, GP120 is encoded by the ov gene, okay. So GP120 changes confirmation and then that conformational change. So the express is a binding side for like CCR5 or CXR4, okay. And then when GP120 binds to those two things I just mentioned, you have a tight binding interaction that draws GP41 closer to the cell that's about to be infected, okay. And then that GP41 fuses with the cell and it so happens that you can block GP41 with a drug known as infovertide, okay. It's a fusion inhibitor. Alternatively, you can also block CCR5, okay. CCR5 is a chemokiner receptor. You can block that with maravirac, okay. And one nifty step one question they could ask is making sure you check that a person has a CCR5 tropic virus before you give like maravirac, same business with infovertide. In fact, maravirac and infovertide only work in HIV1. They do not work in HIV2, just a high yield tidbit to know for your exam. So the HIV virus, unfortunately, for you gets into the cell, okay. Viruses usually have like some kind of coats, so they remove the air blizzard if you will, so they are on coat, okay. And because it's a single stranded RNA virus, it needs to be converted to DNA to have the ability to integrate into the genome. So that's done by reverse transcript things. Remember, reverse transcript phase is an RNA-dependent DNA polymerase, okay. Which can be inhibited by NRT Is, like lamyviodine or zydoviodine.

So these are basically DNA polymerase inhibitors, okay. But the DNA polymerase in this case is RNA-dependent, okay. And lamyviodine zydoviodine, I just put those there to show you that those are NRT Is. And I'll call your attention to the fact that lamyviodine also is used to treat the

Hemorrhagic cystitis secondary to BK virus (BK virus).

Varicella Zoster Virus (VZV).

EBV stays latent in B cells; CMV stays latent in mononuclear cells.

Rabies virus (Rabies).

VZV lesions show vesicles in different stages of healing and a dermatomal distribution; Molluscum contagiosum has central umbilication.

Dynein.

Intra-nuclear inclusions (detects HHV1, 2, and 3).

Congenital CMV; Periventricular calcifications.

Respiratory droplets.

HHV-8; Finding a large number of lymphocytes in the biopsy suggests HHV-8/Caprocystochoma.

HSV-1 leaves nodes in the trigeminal ganglia; HSV-2 leaves nodes in the sacral ganglia.

NRT Is (e.g., Lamivudine); Targets RNA-dependent DNA polymerase.

Intra-nuclear inclusions (detects HHV1, 2, and 3).

Congenital CMV; Periventricular calcifications.

Respiratory droplets.

HHV-8; Finding a large number of lymphocytes in the biopsy suggests HHV-8/Caprocystochoma.

HSV-1 leaves nodes in the trigeminal ganglia; HSV-2 leaves nodes in the sacral ganglia.

NRT Is (e.g., Lamivudine); Targets RNA-dependent DNA polymerase.