Viruses Flashcards
What does it mean for a virus to be “positive sense”?
Similar to an mRNA, it is ready for translation and does not need to bring along extra machinery (solely uses host machinery)
In general, all positive-sense RNA viruses replicate in the cytoplasm
CSF findings in aseptic (nonbacterial) meningitis
Normal glucose
No organisms
Elevated protein
What are the TORCHeS infections?
Cross the placenta and cause infection in utero —> congenital disease
TOxoplasma gondii Rubella CMV HIV and HSV Syphilis
What does it mean for an RNA virus to be “negative-sense”?
It brings its own RNA polymerase
All negative-sense RNA viruses are single stranded except _____
Reovirus (includes rotavirus and colorado tick fever virus)
What are the segmented viruses?
What is the significance of segmented viruses?
BOAR:
Bunyavirus
Orthomyxovirus
Arenavirus
Reovirus
Segmented viruses undergo antigenic variation
What are the 2 types of mutations associated with antigenic variation of viruses?
Antigenic shift: reassortment of different combos of HA and NA leading to new species; associated with PANDEMICS
Antigenic drift: point mutations in HA or NA, associated with epidemics (this is the reason for new flu shot each year)
Why is aspirin contraindicated in kids with suspected viral illnesses? What is the pathogenesis?
Can lead to Reyes syndrome — characterized by fever, rash, vomiting, liver failure, and encephalitis (can be fatal)
Result of OxPhos uncoupling in hepatocyte mitochondria
Where do viruses replicate in host cells?
In general, DNA viruses replicate in the nucleus and RNA viruses replicate in cytoplasm
T/F: all herpesviruses are enveloped
True
General characteristics of Picornaviridae family of viruses
Positive sense RNA virus
Naked (lack viral envelope)
Translated into polyprotein product and viral proteases cleave into infectious subunits
Transmission of Picornaviridae family of viruses
Fecal-oral (EXCEPT rhinovirus which is respiratory droplets)
3 clinical subgroups of Picornaviridae
Hepatitis A —> HSM
Enteroviruses (poliovirus, coxsackie A and B, echovirus)
Rhinovirus —> common cold
Is poliovirus acid-stable or acid-labile? What does this mean for pathogenesis?
Acid stable — survives in GI tract and infects Peyer’s patches (takes 2-3 weeks)
Then spreads to anterior horn of spinal cord causing asymmetric paralysis (often of LEs)
Also causes myalgias, decreased DTRs, aseptic meningitis, and respiratory insufficiency due to paralysis of diaphragm
Clinical manifestations of type A coxsackie virus
Hand, foot, and mouth disease
Red, vesicular rash
Aseptic meningitis
Infection more common in summer months
Clinical manifestations of type B coxsackie virus
Dilated cardiomyopathy
“Devil’s grip” (Bornholm’s disease/pleurodynia) — unilateral, sharp, lower chest pain —> difficulty breathing
Is Rhinovirus acid labile or acid stable? What does this mean for its pathogenesis?
Acid labile — cannot survive GI tract. It is transmitted via inhalation - which may occur via fomites (on dirty hands)
Virus attaches to ICAM-1
The virus also grows best in cooler temps (33 C), so it colonizes upper respiratory tract which acts like an air conditioner
Besides being positive sense RNA, naked, fecal-orally transmitted virus, what are some other characteristics of Hepatitis A virus in terms of acid stable vs. labile, and how humans come into contact with it?
Acid stable
Shed in feces, so it can contaminate the water supply in developing countries. In developed countries, it can be found in uncooked shellfish that were caught in contaminated water from developing countries.
It is commonly seen in traveler’s to endemic areas
Clinical features of Hepatitis A
Often clinically silent, can even be anicteric (kids usually present this way)
Active infection = fever, hepatomegaly, jaundice; symptoms last roughly 1 month
There is no carrier or chronic state
Note that smokers with Hep A develop aversion to tobacco
Characteristics of Caliciviridae (norovirus)
Positive sense ssRNA virus
Naked
Produces long polyprotein - cleaved into infectious subunits by viral proteases
Where is norovirus commonly found and what is its clinical presentation?
Often occurs with many people in close quarters — 90% of cruise ship diarrheal illness! Also occurs in daycare, schools, or with consumption of shellfish at buffets.
Causes viral gastroenteritis —> explosive, watery diarrhea
Characteristics of Flaviviridae family of viruses
Positive sense RNA virus
Enveloped
Non-segmented
What diseases are caused by the Flaviviridae family of viruses?
Hepatitis C
Dengue fever
Yellow fever
West Nile Virus
Characteristics of Dengue fever
Vector = aedes mosquito
Infects bone marrow; 4 types of Dengue, but type II is most important — known as “break-bone fever”
Causes thrombocytopenia and subsquent bleeding, so it is a hemorrhagic fever. Can eventually lead to renal failure and death
Vector and Clinical presentation of Yellow fever
Vector = aedes mosquito
Causes jaundice, backache, bloody diarrhea, hematemesis
Clinical features of West Nile virus including reservoir and vector, major complication, and diagnosis
Reservoir = birds Vector = mosquitos
Major complication = encephalitis; also causes myelitis leading to flaccid paralysis, seizures, and coma
Dx by PCR and serology
Hepatitis C, belonging to the Flaviviridae family, is a positive sense RNA virus and is enveloped. What is its mechanism of transmission?
Most common method of transmission is via exposure to infected blood — can be through blood transfusion, IV drug use/needle-sharing, accidental needle-sticks, etc.
Can also be transmitted across placenta, sexual transmission (although Hep B is more common this way), or breastfeeding
What allows for antigenic variation of Hepatitis C virus if it is non-segmented?
It has no proofreading 3-5 exonuclease activity in viron-encoded RNA polymerase, so there are frequent mutations
Clinical findings in Hepatitis C infection
Acute: jaundice, RUQ pain, hepatomegaly, increased liver enzymes (ALT will rise and fall within 6 months)
Chronic (note that 60-80% of cases become chronic): cirrhosis, hepatocellular carcinoma
Associated with cryoglobulins = serum proteins containing IgM that precipitate in cool temps
Characteristics of Togaviridae family (equine encephalitis, rubella)
Positive sense RNA virus
Enveloped
Long polyprotein precursor cleaved by proteases into infectious subunits
Most are arboviruses = arthropod vector (mosquitos)
Rubella is spread by respiratory droplets and has 3 different clinical presentations: neonatal, childhood, and adult. What is the classic triad of neonatal rubella?
Sensorineural deafness
Cataracts
Patent ductus arteriosus
[note that rubella also causes mental retardation, microcephaly, blindness, jaundice, pulmonic stenosis, purpuric blueberry muffin rash, and radiolucent bone lesions in neonates]
Rubella is spread by respiratory droplets and has 3 different clinical presentations: neonatal, childhood, and adult. What is the childhood presentation?
Starts as postauricular and occipital tender LAD + fever
Childhood exanthem = maculopapular rash - starts on face and moves downward, typically present 3 days
Rubella is spread by respiratory droplets and has 3 different clinical presentations: neonatal, childhood, and adult. What is the adult presentation?
Fever
Arthralgia
Arthritis
[note that rubella is more commonly seen in immigrants because they may not be immunized]
Characteristics of coronaviridae (coronavirus); what is unique about this virus??
Positive sense RNA virus
Encapsulated with helical shaped capsule = unique!
Clinical manifestations of coronavirus infection
Can cause common cold or acute bronchitis leading to ARDS
Can cause SARS or MIRS (dx by SARS Abs or PCR)
Characteristics of HIV (retrovirus)
ssRNA positive sense virus - gets converted into DNA intermediate using RT —> gets incorporated into host chromosomes —> replicates indefinitely
Enveloped
Diploid — 2 molecules of +strand RNA in each virion
What are the 3 important genetic components of HIV?
gag = p24 — capsule for RNA strands
env = gp41 (transmembrane protein) and gp120 (outer glycoprotein)
pol = reverse transcriptase
Describe pathogenesis and clinical features of HIV once it has infected host cells
Initially infects macrophages — leads to prodrome of flu-like symptoms including cervical LAD and fever lasting several weeks, affecting CD4 cells.
Can be latent for up to 10 years, followed by steep decline in CD4 cells at which time it is considered clinical AIDS (CD4 <200)
HIV gains entry to host cells via ____ in early stages, or ____ in late stages
CCR5; CXCR4
What type of cancer is associated with HIV?
Diffuse, large B cell lymphoma
How is HIV diagnosed?
ELISA (may get false negative so serial tests are needed)
Confirm with Western blot
Measure viral load and CD4 count via PCR
[test neonates using HIV-RNA and HIV-DNA nucleic acid amplification test, otherwise will always come up positive d/t mom’s antibodies]
Characteristics of influenzavirus (orthomyxoviridae); what is unique about this virus?
Negative sense RNA
ONLY RNA VIRUS THAT REPLICATES IN THE NUCLEUS
Enveloped 8 segments (antigenic variation)
What is the difference between influenza A and B in terms of antigenic variation?
A is most important because it undergoes both antigenic DRIFT and SHIFT, thus it is the cause of epidemics and pandemics
B undergoes just antigenic DRIFT, so it is associated with endemics
In a viral infection such as H1N1, what does the “H” stand for? What is the pathogenesis mechanism?
What does the N stand for?
Hemagluttinin — glycoprotein that binds sialic acid on red cells (H1, H2, and H3 in human infection); H determines cell tropism (which cells virus can bind to).
Path: Once HA has bound to a cell, it is endocytosed. The pH of the cell is then adjusted by M2 protein for viral uncoating. After replicating in the nucleus, neuraminidase (this is the N!) cleaves sialic acid to release virions
How is influenzavirus (orthomyxoviridae) transmitted? What complications are associated with it?
Respiratory droplet transmission — typical season is Dec—>Feb, so vaccine is recommended in Oct
Major complication = pneumonia (often associated with S.aureus infection)
Also associated with Guillain Barre syndrome —> ascending paralysis
What would CSF show in the ascending paralysis associated with GBS?
Albuminocytologic dissociation = High protein, Low WBC
Characteristics of paramyxoviridae (measles, mumps, RSV, parainfluenza viruses), including mechanism of transmission
Negative sense RNA viruses
Enveloped
Can have any combo of virulence factors: HA, NA, fusion protein
Transmitted via respiratory drops
Clinical manifestations and major complications associated with Measles (rubeola) including timeline
Prodromal: 4 C’s — cough, coryza (runny nose), conjunctivitis, Koplik spots (small blue-white on red background on buccal mucosa)
High fever lasting 4 days (104 F); 1-2 days after appearance of Koplik spots you see maculopapular rash - starting on face/forehead and progressing downward (likely confluent)
Major complications = pneumonia, subacute sclerosing panencephalitis (SSPE) - dx by anti-measles Ab
What virulence factors are associated with measles (rubeola) virus?
HA and fusion protein
What vitamin reduces measles morbidity and mortality?
Vitamin A
What does the “fusion protein” do as a virulence factor associated with paramyxoviruses?
Forms syncytia — multinucleated giant cells (i.e., in lymphoid tissue in measles)
Clinical features and virulence factors associated with mumps infection (paramyxoviridae)
Parotitis, orchitis (can progress to epididymal inflamm. - typically unilateral)
Complication = meningitis
VF’s: HA, NA, fusion protein (all 3!)
Clinical features and virulence factors associated with respiratory syncytial virus (RSV, paramyxoviridae)
Seen in infants <6 mos
Attaches to G protein to infect respiratory epithelial cells —> bronchiolitis, PNA (MCC in infants), rhinitis, pharyngitis
VF’s: fusion protein only! (No HA or NA!!)
Clinical features and virulence factors of parainfluenzavirus (paramyxoviridae)
Croup = laryngotracheobronchitis
Mainly affects kids — Characteristic seal-bark cough and inspiratory stridor. CXR “steeple sign” — narrowing of subglottic region
Causes severe cold in adults
VFs: HA, NA, and fusion protein (all 3!)
Characteristics of Rhabdovirus (rabies)
Negative sense RNA virus
Enveloped (bullet shaped on electron microscopy)
Helical capsid
Zoonotic — most common carrier in US is bats, but also found in rodents, foxes, skunks, etc
Pathogenesis and clinical symptoms of rabies (rhabdovirus)
Envelope glycoprotein binds nicotinic ACh receptors in post-synaptic motor end plate, then over period of weeks to months it spreads along peripheral nerves in retrograde fashion while replicating in motor neurons.
It eventually travels to dorsal root ganglia, then to brain
Symptoms include fever, rabies encephalitis, and increased parotid secretions
Diagnostic feature of rabies (rhabdovirus)
Eosinophilic Negri bodies (inclusions in hippocampus cytoplasm - in pyramidal cells)
Negri bodies also found in purkinje cells
Characteristics of Filoviridae (ebola and marburg viruses)
Negative sense RNA virus
Helical capsid
Enveloped
Marburg virus and Ebola virus cause similar symptoms — what are they?
How to people get these viruses?
Hemorrhagic fever
Petechial rash
Death typically occurs due to blood loss —> hypovolemic shock —> end-organ failure
Caused by contact w/ infected animal (primate, fruit bat) in endemic area like Africa. Also seen in healthcare workers in contact with bodily fluids of infected persons or those who have died from disease
Characteristics of Bunyaviridae (hantavirus, california encephalitis, rift valley fever virus); what is unique about this virus?
Negative sense RNA virus
Enveloped — obtains envelope from golgi body complex of host cells!
3 circular segments
Most are arboviruses (arthropod-borne)
Clinical features of hantavirus (Bunyaviridae)
Reservoir = deer mouse
Transmitted via rodent urine/feces
Causes pulmonary capillary leak, pre-renal azotemia, and hemorrhagic fever
Clinical features of California Encephalitis virus and Rift Valley Fever virus
Aedes mosquito spread
Cause seizures and encephalitis
Characteristics of Arenaviridae (lymphocytic choriomeningitis); what is unique about this virus?
Negative sense RNA virus (note that it has the potential to be positive or negative sense and is thus considered AMBISENSE)
Enveloped
Helical capsid
2 segments (Ag variation)
Sandy/grainy appearance on electron microscopy
What viruses have helical capsids?
Arenaviridae
Filoviridae
Rabdoviridae
Clinical presentation of Arenaviridae
Lymphocytic choriomeningitis = febrile, aseptic meningoencephalitis
Rodent transmission
Reoviridae characteristics (rotavirus, colorado tick fever virus); why is this virus unique??
Double-stranded RNA virus!! (So it is both positive and negative sense)
Naked
9-12 segments (typically 11)
Clinical features of rotavirus (Reoviridae)
NSP4 enterotoxin causes secretory (watery) diarrhea by increasing Cl- permeability
Most common in wintertime; higher risk in kids (MCC of severe diarrhea)
Clinical features of Colorado Tick virus (reoviridae); how is this virus differentiated from a Rocky Mtn Spotted Fever infection?
Vomiting, fever, myalgia
Differentiate from RMSF because Colorado Tick virus does NOT present with a rash!
Characteristics of HSV 1 and 2 (herpesviridae) including mode of transmission
Linear dsDNA virus
Enveloped
Transmission via sex, saliva, or vertical (this is a TORCH infection!)
Characteristic findings on electron microscopy for HSV 1 and 2; what other viruses are these seen in?
Intranuclear inclusion bodies (Cowdry bodies)
Also seen in CMV and VZV
Clinical features of HSV type 1
First sign of infection = gingivostomatitis, eventually just herpes labalis (cold sores)
Keratoconjunctivitis —> serpiginous corneal ulcers on slit lamp exam
Temporal lobe encephalitis — typical encephalitis findings but with bizarre behavior and personality changes
Where does HSV 1 vs. HSV 2 remain latent/dormant?
HSV 1 = latent in trigeminal ganglia
HSV 2 = latent in sacral ganglia
Describe appearance of herpes rash; what is herpetic whitlow?
Herpes rash has “dew drops on a rose” appearance
Herpes whitlow = herpes rash on the finger, may be caused by type 1 or type 2; seen in dentists
Type of rash seen in both HSV type 1 and 2, but more common in type 1; occurs 1-2 weeks after infection
Erythema multiforme
Clinical features of HSV-2 including methods for dx
Causes herpes genitalis
Painful inguinal LAD, painful vesicular ulcerations
May cause aseptic meningitis in adults and adolescents
Dx: PCR or Tzank smear for multinucleated giant cells
Characteristics of EBV (herpesviridae) including site of latency
dsDNA virus
Enveloped
Remains latent in B cells (EBV envelope glycoprotein binds CD21 to infect B cells)
Clinical features of EBV; what happens if these patients are given amoxicillin or ampicillin?
Causes infectious mononucleosis - transmission via saliva
Fever, tender LAD, splenomegaly d/t T cell proliferation, pharyngitis with copious tonsillar exudate
If misdiagnosed as strep pharyngitis and given abx — can develop maculopapular rash
Dx of EBV mononucleosis
Reactive CD8+ CTLs seen on blood smear (aka Downey or atypical cells) — can also be NK cells
Can also use Mono spot test for rapid dx
What disease can EBV cause in HIV pts?
Oral hairy leukoplakia — not a cancerous lesion!
May look like candida but it cannot be scraped off the tongue
What 3 cancers are those with EBV predisposed to?
B cell lymphomas:
Hodgkins — Reed-Sternberg cells look like “owl eyes”
Non-Hodgkins — endemic or African Burkitt lymphoma - large jaw lesion+swelling
Nasopharyngeal carcinoma (more common in asian population)
NOTE that owl-eye inclusion bodies are characteristic of CMV, not EBV
Characteristics of CMV (herpesviridae) including site of latency
dsDNA virus
Enveloped
Latent in B and T cells, as well as macrophages (all mononuclear leukocytes) — reactivated by immunosuppression
Manifestations of CMV as a result of TORCH infection
Note that 80-90% are asymptomatic, but may develop unilateral hearing loss later on.
Blueberry muffin rash (same as is seen with congenital rubella) including thrombocytopenia and petechial hemorrhage
Structural changes in brain include intracranial calcifications (periventricular or parenchyma itself) leading to mental retardation and seizures, may also see ventriculomegaly
Also HSM, jaundice, and sensorineural hearing loss (MCC)
What condition can CMV cause in pregnant women (other than TORCH infection)
Hydrops fetalis
Transplant patients are most susceptible to what clinical manifestation of CMV? How is this diagnosed?
Pneumonia; diagnosed via buffy coat culture
AIDS pts are most at risk for CMV with CD4+ counts of what?
What are the major clinical manifestations of CMV in AIDS pts?
CD4 < 50
Most common manifestation = CMV retinitis (typically unilateral)
Esophagitis with deep, linear ulceration (differentiate from herpes which has multiple shallow ulcerations)
CMV colitis with ulcerated walls
The most common clinical presentation of CMV in those who are NOT immunocompromised is CMV mononucleosis, which presents the same as EBV mono. What is the one diagnostic difference?
CMV mono spot test will be negative
Characteristics of varicella zoster virus (herpesviridae) including diagnostic test and site of latency
dsDNA
Enveloped
Dx: Tzank smear shows multinucleated giant cells
Latent in dorsal root ganglia of nerves
Clinical features of chickenpox caused by VZV
Fever, headache, widespread pruritic rash composed of vesicular lesions with “dew drops on a rose” appearance
Transmission via respiratory droplets or material from exanthem itself
How would you differentiate chickenpox rash from smallpox?
VZV rash will have lesions at different stages of healing, while smallpox will all be same age
Adult presentation of VZV infection
Pneumonia, encephalitis (note that these can be presentations in kids too)
Adults typically contract in immunocompromised state
VZV lies dormant in dorsal root ganglia. It may be reactivated with aging, stress, or immunocompromised state and cause what disease? What are the clinical features?
Shingles (herpes zoster)
“Dew drops on a rose” rash in dermatomal distribution (rarely crosses midline — if it does you must test for HIV); extremely painful and can persist as post-herpetic neuralgia
Shingles (herpes zoster) typically affects the dermatomes in the thoracic region, but it may have a more dangerous distribution in immunocompromised - causing what complication?
Shingles may affect trigeminal V1 —> herpes zoster ophthalmicus resulting in unilateral vision loss
Describe effects of VZV acquired as a TORCH infection
Causes congenital varicella syndrome
Limb hypoplasia
Cutaneous scarring in dermatomal pattern
Blindness
Characteristics of HHV-6 (herpesviridae) including what cells it infects and what disease it causes
dsDNA virus
Enveloped
Infects CD4+ cells
Causes Roseola (aka Sixth disease aka exanthem subitem)
Clinical features of roseola (HHV6 herpes viridae)
Typically affects kids age 6 mos-2 years; usually self-limiting
4 days of fever (over 104 F) —> febrile seizures
Once fever subsides, get diffuse lacy body rash that spares the face
Characteristics of HHV-8, Kaposi’s sarcoma (herpesviridae) including transmission and cells it infects
dsDNA virus
Enveloped
Transmission via saliva (high risk = men who have sex with men, Russian men, African populations)
Can infect B cells —> primary effusion B cell lymphoma
Clinical features of HHV-8, Kaposi’s sarcoma (herpesviridae)
Violacious lesions on nose, extremities, and mucous membranes (hard palate, GI tract) d/t dysregulation of VEGF —> angiogenesis
HHV-8, Kaposi’s sarcoma (herpesviridae) may be confused with bacillary angiomatosus (bartonella hensleae bacterial infection). How are these 2 differentiated?
Need to examine lesions microscopically to differentiate:
Kaposi’s has lymphocytic infiltrate while bacillary angiomatosus would show neutrophilic infiltrate
Characteristics of Polyomaviridae (JC polyomavirus, BK polyomavirus)
Circular dsDNA viruses
Naked
Clinical manifestations of JC virus (polyomaviridae) including diagnostic feature
Progressive Multifocal Leukoencephalopathy (PML) — demyelination d/t killing of oligodendrocytes
Affects immunocompromised and AIDS CD4<200
Dx: non-enhancing multifocal brain lesions in white matter
Clinical manifestations of BK virus (polyomaviridae) including patient population this is seen in
Nephropathy
Hemorrhagic cystitis
Often affects kidney and bone marrow transplant patients
Characteristics of papillomaviridae (HPV 6,11,16,18,31,33)
dsDNA virus
Naked
Most common STD according to sketchy
Clinical manifestation of HPV1-4
Verruca vulgaris = cutaneous common wart; transmission via physical contact
Clinical manifestations of HPV-6 and HPV-11
Laryngeal papillomatosis (recurrent respiratory papillomatosus) = airway tumors in kids, thought to be transmitted during vaginal birth
Anogenital warts (condyloma accuminata) via sexual transmission
Clinical manifestations of HPV-16, 18, 31, and 33
Anogenital cancers (squamous cell carcinomas — bc virus infects squamous cells)
Considered AIDS-defining cancers
Note that cervical cancer may present as post-coital bleeding; can screen for this via pap smear looking for koilocytes
Describe carcinogenesis of HPV
p53 targeted by E6 protein (can’t arrest cell cycle at G1/S)
Rb targeted by E7 protein (Rb is tumor suppressor)
Characteristics of parvovirus B19 (parvoviridae); what is unique about this virus?
ssDNA virus !!! (Also smallest DNA virus)
Naked
Transmission of parvovirus B19 (parvoviridae)
Respiratory droplets or vertical transmission (TORCH infection!)
TORCH —> hydrops fetalis in utero
Clinical manifestations of parvovirus B19
How do adults present? How do sickle cell pts present?
Slapped cheek fever (aka Fifth disease aka erythema infectiosum): 1 week of low grade fever; fever breaks and is followed by rash that begins on face and moves downward
Adults present with joint pain, arthritis, and edema
Sickle cell patients present with aplastic anemia (d/t depletion of bone marrow)
Characteristics of adenovirus (adenoviridae) including transmission
dsDNA virus
Naked
Transmission via respiratory droplets or fecal-oral (commonly occurs in kids, military recruits, and people swimming in public pools)
Clinical manifestations of adenovirus (adenoviridae)
MCC of tonsilitis and adenoiditis
Hemorrhagic cystitis (presents as gross hematuria)
Common cause of viral conjunctivitis (pink eye)
Characteristics of poxviridae family (smallpox, cowpox, molluscum contagiosum); what is unique about this virus?
dsDNA virus
Dumbbell shaped core
Virions contain all its own machinery! So it makes its own envelope.
Only DNA virus that completely replicates in cytoplasm, using DNA-dependent RNA polymerase
What diagnostic feature is found on biopsy of poxviridae-associated lesions?
Guarnierni bodies = cytoplasmic inclusion bodies indicative of sites of viral replication
The discovery of cowpox is why we now have a vaccine for smallpox. What are the clinical features of smallpox?
Raised blistering lesions similar to chickenpox, but all lesions are same age!
Clinical features of molluscum contagiosum (poxviridae)
Flesh-colored, dome-shaped, umbilicated (dimpled) skin lesions that are usually found on the trunk (spares the palms and soles!)
Diffuse spread of these lesions typically only occurs in immunocompromised, otherwise may only present with 1 lesion
Characteristics of Hepatitis B virus (hepadnavirus)
Enveloped DNA virus that replicates inside and outside the nucleus
Circular genome that is partially double stranded, uses RT to get to intermediate ssRNA, then becomes fully dsDNA during replication
Transmission of Hep B virus
Sexual transmission, sharing blood products, or during delivery (does not cross placenta)
T/F: Hep B is more likely to become chronic than Hep C
False; Hep C is more likely to become chronic
Hepatitis C is more likely to become chronic than Hepatitis B. What is the exception to this?
Newborns with Hep B have 90% chance of developing chronic infection
Clinical manifestations of Hepatitis B including long term sequelae
Hepatic: RUQ pain, jaundice, hepatomegaly, etc.
Extrahepatic: polyarteritis nodosa, purpuric rash with nonblanching appearance, arthralgia
May cause membranous glomerulonephritis or membranoproliferative glomerulonephritis
Long term sequelae = cirrhosis, hepatocellular carcinoma
Complication of polyarteritis nodosa seen in Hep B infections
Kidney damage
Describe ALT changes in viral infections, and what happens to ALT levels in neonatal hepatitis
ALT is higher in viral infections of the liver
ALT is normal in neonatal hepatitis
Describe diagnostic markers of Hep B infection
First marker of active infection (whether acute or chronic) is HbSAg (Hep B surface antigen), followed by HBeAg
Anti-HBc antibodies are positive during window period
Anti-HBe along with HBs indicate previous infection (not prior immunization)
Anti-HBs indicates recovery (if seen in conjunction with Anti-HBe or HBc), or prior immunization
Characteristics of Hepatitis D virus
Negative sense RNA virus
Circular genome
Enveloped
Hepatitis D requires ______ to be infectious
What is the difference between coinfection and superinfection?
HBsAg (hepatitis B surface antigen)
Coinfection = Hep B and Hep D acquired at the same time
Superinfection = Hep D acquired after Hep B infection —> worse outcomes