RNA viruses – Part II

Alphavirus

Causes some obscure brain infection in a farmer called equine encephalitis. Asked maybe once on an old NBME form somewhere.

Rubella (aka German measles)

Causes fever and head-to-toe maculopapular rash in unvaccinated children (and adults).

HY point about the presentation is that it causes post-auricular and sub-occipital lymphadenophathy.

Adults can get arthritis. For example, if the USMLE gives you a neonate with congenital rubella syndrome + they ask what symptom the woman most likely had when pregnant, arthritis can be an answer if rash is not listed. USMLE will not force you to choose between rash and arthritis. The point is that you merely are aware arthritis is HY in adults as part of the presentation.

Congenital rubella presents as patent ductus arteriosus (PDA) in a neonate. Exceedingly HY / pass-level. Cataracts and deafness also possible.

MMR vaccine is live-attenuated and is contraindicated during pregnancy due to theoretical risk to the fetus. If a woman inadvertently receives the vaccine while pregnant or within the month prior to pregnancy, it is not an indication for abortion, but risks to the fetus are increased and proper monitoring is important.

The vaccine is not contraindicated in HIV. Literature says subjectively can be implemented in patients who are severely immunocompromised with consideration of CD4 count, but there is no specific CD4 cutoff. The point is, MMR vaccine is avoided in pregnancy, but not avoided in HIV.

Hepatitis C

Parenteral; can be acute or chronic.

Transmitted almost exclusively from IV drugs/blood exposure. Not present in breastmilk and non-sanguineous body fluids (in contrast to HepB).

In contrast to HepB, HepC is not considered sexually transmitted. Large longitudinal study of couples with one HepC(+) partner showed sexual transmission almost nil (possibly due to menses exposure). If you’re forced to choose for FM / behavioral science Qs, however, still inform that abstinence or barrier contraception minimizes risk.

Hepatocellular damage is due to T cells / death is due to T-cell-mediated apoptosis, not direct viral cytopathicity. This is the highest yield point for HepC on USMLE.

No vaccine due to ­­ antigenic variation (i.e., >7 genotypes and 80 subtypes of HepC exist).

IgM against HepC means acute infection.

IgG against HepC means usually means chronic HepC.

Many drugs can be used to treat. USMLE doesn’t care. You could in theory be aware of pegylated interferon-a.

West Nile virus

Asked once on an old, offline NBME. USMLE wants you to know it has a bird reservoir and is spread by Culex mosquito.

Presents as flu-like illness in most people. The NBME Q simply gives patient with headache and fever + they say the causal organism is spread by Culex mosquito and has a bird reservoir –> answer = West Nile virus.

Dengue virus

Spread usually by Aedes mosquito.

Causes flu-like illness + thrombocytopenia (bleeding gums, petechiae, etc.) + severe joint and abdominal pain.

Yellow fever virus

Spread usually by Aedes mosquito.

Causes flu-like illness and jaundice (hence yellow fever) due to hepatocellular damage. Councilman bodies are seen on biopsy of the liver, which are apoptotic bodies.

Zika virus

Spread usually by Aedes mosquito.

Causes microcephaly in neonates if mother exposed while pregnant.

Human T-cell lymphotropic virus

Retrovirus similar to HIV.

Causes a cutaneous T-cell lymphoma, known as mycosis fungoides, which appears like a skin rash.

Mycosis fungoides

If this extends to the blood as a T-cell leukemia, it is now called Sezary syndrome. Sezary syndrome usually presents with diffusely red skin, called erythroderma.

Sezary syndrome

Both mycosis fungoides and Sezary syndrome are characterized by cerebriform-shaped cells on light microscopy.

HTLV can also cause an obscure condition called tropical spastic paraparesis, which is antibodies against neuronal cells leading to otherwise unexplained neurodegeneration over weeks to months.

Hepatitis D

Requires hepatitis B in order to infect, which can be due to co-infection (happening at the same time) or superinfection (occurs later in someone who already has HepB).

If USMLE asks how to prevent HepD infection, answer = vaccination against hepatitis B. There is no vaccine against HepD.

Apparently HepB antigen forms the envelope for HepD (i.e., forms a circle around HepD).

Human immunodeficiency virus (HIV)

Invades and destroys CD4+ T cells.

Transmitted via blood, IV drug use, and sexually. Also present in breastmilk.

Highly active anti-retroviral therapy (HAART) consists of three drugs: two nucleoside reverse-transcriptase inhibitors (NRTI) + either a non-nucleoside reverse-transcriptase inhibitor (NNRTI) or protease inhibitor.

Pharmacology for HIV is lengthy and involved, so if you want in depth discussion of all of the drugs, you can open as a separate tab my HIV pharm module here.

HAART therapy is initiated immediately upon diagnosis of HIV. We do not wait for CD4 count to fall to a certain level before commencing.

Once CD4 count falls below 200/μL, patients are started on trimethoprim/sulfamethoxazole (TMP/SMX) for Pneumocystis jiroveci pneumonia (PJP) prophylaxis.

NBME has Q where they give you an HIV patient with CD4 count of, e.g., 550, and then ask what type of drug regimen needs to be commenced. Answer in this case is “three drug anti-retroviral therapy alone,” where “three drug anti-retroviral therapy + Pneumocystis prophylaxis” is wrong, as well as all answers that say two-drug regimen.

HIV patients with CD4 counts under 200, or those who get any HIV-related opportunistic infection, are said to have Acquired Immunodeficiency Syndrome (AIDS).

Toxoplasmosis comes in with CD4 count under 100. Prophylaxis is TMP/SMX, the same as for PJP, so often times, once TMP/SMX is appropriately commenced at CD4 of 200 for PJP, it’s already “two birds with one stone,” so we don’t have to worry about Toxo prophylaxis later.

However the treatment for Toxo is sulfadiazine + pyrimethamine. For Pneumocystis TMP/SMX is both the prophylaxis and treatment. NBME asks the Tx for toxo on one of the forms, where TMP/SMX is also listed and wrong. So you need to know the prophylaxes + treatments for Toxo and PJP.

Under CD4 counts of 50-100, Mycobacterium avium intracellulare and CMV infections can occur. MAI causes lung infections similar to TB, and also sometimes GI infections. CMV causes retinitis. Blurry vision in an HIV patient is CMV retinitis till proven otherwise.

In addition, progressive multifocal leukoencephalopathy (PML; neuronal degeneration caused by reactivation of JC polyoma virus), primary CNS lymphoma, and AIDS complex dementia (presents as wet, wobbly, wacky, similar to normal pressure hydrocephalus) can occur at CD4 counts <50-100.

The USMLE might give you a patient with CD4 count of 47 who has ring-enhancing lesion of the brain who is taking HAART and TMP/SMX. Diagnosis is primary CNS lymphoma; Toxo is wrong. The way we know Toxo is wrong is because the patient is on TMP/SMX, which is the prophylaxis for both Pneumocystis and Toxo. Commencing TMP/SMX at a CD4 count of 200 for PJP, as I already said, is “two birds with one stone” by the time the patient gets to CD4 of 100, which is when Toxo comes in. It’s only patients who aren’t on TMP/SMX by the time they fall to CD4 of 100 who get Toxo.

Causes Cryptococcal neoformans meningitis, which presents with low glucose, high protein, and high lymphocytes. Diagnosed with CSF latex agglutination (most accurate), or India ink prep, or mucicarmine staining.

Adults with severe acute-onset seborrheic dermatitis, disseminated scabies, or molloscum contagiosum should have an HIV test.

HIV increases risk of squamous cell carcinoma in MSM.

HIV can cause focal segmental glomerulosclerosis (FSGS), a nephrotic syndrome. When HIV leads to renal disease, it is called HIV nephropathy. It is almost always FSGS.

HIV can lead to chronic diarrhea caused by Cryptosporidium parvum, whereas immunocompetent patients clear it. C. parvum is a protozoan (unicellular eukaryote).

Can be a cause of anemia of chronic disease (low Hb, low iron, normal ferritin).

Patients with HIV require Pap smear at time of diagnosis, and then every year (annually) thereafter (asked on Obgyn forms). Normally, Paps are performed every three years from age 21, and then every 5 years from age 30 with HPV co-testing.

To prevent vertical transmission, the most important measure to take is HAART therapy while pregnant + keeping the mother’s viral load as low as possible. She will then receive intrapartum zidovudine, C-section is performed, and then the neonate will receive 6 weeks of zidovudine commenced within 12 hours of birth. Some students will get pedantic about various alternative/updated regimens for neonates, but one of the NBMEs assesses this point about 6 weeks of zidovudine commenced within 12 hours of birth.


1. What is the taxonomy/categorization of hepatitis C?

2. How is West Nile virus spread?

What is its reservoir?

3. Low hemoglobin in HIV patient. Most likely cause?

What do you expect for iron and ferritin levels?

4. Which neonates notably get patent ductus arteriosus?

5. If patient has CD4 count of 550, should we start HAART therapy, Pneumocystis prophylaxis, or both, or neither?

6. How do we prevent vertical transmission of HIV from mother to fetus?

7. How is HepC transmitted?

8. HIV patient with CD4 count of 50 has neuronal degeneration over weeks to months. What is the most likely infective organism and diagnosis? (not HIV)

9. Stiff neck, fever, and photophobia in HIV patient with CD4 of 180. Diagnosis?

10. Which virus is most taxonomically similar to HTLV?

11. What is the taxonomy/categorization of alphavirus?

12. What are three “unusual” patient groups who require an HIV test?

13. Which virus causes post-auricular and sub-occipital lymphadenopathy?

14. What spreads West Nile virus?

How does it present?

15. What is the taxonomy/categorization of West Nile virus, Zika, yellow fever, and dengue?

16. How does rubella present in children vs adults?

What about congenital rubella?

17. What is the taxonomy/categorization of hepatitis D?

18. What is HAART therapy for HIV? How many drugs should be given?

At what CD4 count is it commenced?

19. When is an HIV patient considered to have AIDS?

20. How often do Pap smears need to be performed in HIV?

21. Why is there no vaccine against HepC?

22. AIDS patient with CD4 count of 47 is on HAART and TMP/SMX prophylaxis for PJP. He develops a seizure. CT of the head shows a ring-enhancing lesion. Diagnosis?

23. What renal condition is HIV notably associated with?

24. What kind of vaccine is rubella?

What type of patient demographic is it contraindicated in?

25. At what CD4 count is Pneumocystis prophylaxis initiated?

What is the prophylaxis and treatment of Pneumocystis?

26. What spread dengue virus?

How does dengue present?

27. What is the cause of hepatocellular damage in HepC?

28. AIDS patient who presents with gait ataxia, urinary incontinence, and personality change. What’s the diagnosis?

29. What spreads Zika virus?

What does Zika notably cause?

30. What is special about hepatitis D infectivity?

What is the best way to prevent it?

31. What is the taxonomy/categorization of HIV?

32. At what CD4 count in HIV do we worry about Toxoplasmosis?

What is the prophylaxis and treatment of Toxo?

33. What are three conditions HTLV causes?

What do we see on light microscopy?

34. What are mycosis fungoides and Sezary syndrome?

35. What is the taxonomy/categorization of rubella?

36. Which organism classically causes chronic diarrhea in HIV?

37. At what CD4 counts do we worry about MAI and CMV in HIV?

What do these infections cause?

38. What is the taxonomy/categorization of HTLV?