DNA Virus section provides High Yield Information needed for USMLE, COMLEX, Medical School, Residency, and as a practicing Physician.
Table Of Contents
Reovirus
- Features:
- Types of Reovirus:
Rotavirus
- Features:
- Most common type of Reovirus
- dsRNA- replicates in cytoplasm
- Naked
- Segmented virus
- Transmission:
- fecal oral
- Clinical presentation:
- – Toxic mediated secretory diarrhea- may be explosive watery diarrhea
- Toxin:
- – NSP4- increases Cl permeability–> secretory diarrhea
- Seasonal virus:
- usually winter
- Population at risk:
- – Children: high risk
- *Number 1 cause of severe diarrhea in children**
- Treatment:
- – Supportive care
- – Oral rehydration therapy
- Vaccine:
- – Live attenuated
- ORAL
- – First dose: <3 months old
- – Live attenuated
- Vaccine increases risk of:
- – intussusception
Herpes Simplex Virus: HSV1 and HSV2
- Features:
- DNA virus
- – Replicates in nucleus
- – Double stranded and linear
- Enveloped
- Intra-nuclear inclusions/Cowdry bodies
- Herpes simplex part of herpes virus family
- DNA virus
- Transmission:
- – Sex
- – Saliva
- – Vertical transmission (part of TORCHeS)
- 2 strains of herpes simplex:
- HSV1:
- – usually confined to upper half of the body
- Clinical Presentation:
- – Gingival stomatitis: painful and aggressive: commonly seen in infants:
- Causes: widespread inflammation of lips and gums
- Gingival stomatitis will heal and look like cold sores/ulcers on lips–> Herpes labialis
- – Herpes labialis: most common infection of mouth
- – Keratoconjunctivitis: serious eye infection.
- – Associated with temporal lobe encephalitis: causes hemorrhage and necrosis of inferior and medial temporal lobes
- Presentation of temporal lobe encephalitis
- – seizure
- – headache
- – fever
- – altered mental status
- – bizarre behavior
- – olfactory hallucinations
- – personality changes
- HSV1: most common cause of sporadic encephalitis
- HSV1 virus remains latent in trigeminal ganglia – reactivated by stress or immunocompromised state
- Rash: “Dew drops on rose petals” appearance
- – Clear vesicles sitting on top of erythematous base
- Herpetic whitlow
- – Herpes vesicles on fingers
- – Due to HSV1 and HSV2
- – More commonly seen in dentists because their hands are in patients’ mouths
- – Erythema multiforme
- HSR-> small target lesions on back of hands and feet and moves centrally
- Rash appears 1-2 weeks after infection
- HSV2:
- – More common in lower half of the body- genitalia
- Causes:
- – Herpes genitalis: painful LAD with clusters of vesicles with a red base
- Transmission:
- – Sexual
- – Obstetric
- HSV2 remains latent in Sacral ganglia
- Associated with Aseptic Meningitis in adolescents and adults
- HSV1:
- Diagnosis:
- – PCR: test of choice for Dx
- – Scraping ulcer base and using Tznak smear
- Treatment:
- – None
- – Prevention of breakouts: Acyclovir, Valcyclovir
Ebstein-Barr virus (EBV)
- Features:
- dsDNA virus
- Causes:
- Infectious mononucleosis
- Transmission:
- saliva
- Clinical presentation:
- – Fever
- – Tender LAD generally posterior cervical region, can get generalized LAD
- – Splenomegaly
- – Pharyngitis
- EBV pharyngitis
- – commonly seen in teens and adults
- – pharyngitis and tonsilar exudates
- Transmission of virus:
- targets B lymphocytes, remains latent in B cells
- – If EBV is accidentally treated with Amoxicillin or Ampicillin
- Develops a maculopapular rash
- EBV increase risk for cancer
- – B cell lymphoma: Burkitt lymphoma and Nasopharyngeal carcinoma
- – Oral hairy leukoplakia
- Diagnosis:
- – Acute infection: Activation of B cells: Use heterophile, antisheep red cell Ab- diagnose mono
- – Mono spot test:
- rapid diagnosis, IgM
- Treatment:
- – Supportive therapy
- – Avoid contact sports due to risk of splenic rupture
Cytomegalovirus (CMV)
- Features:
- dsDNA: replicates in nucleus
- Herpes virus family
- Remains latent in cells: lymphocytes, monocytes, macrophages
- Reactivated when immunosuppressed
- Transmission:
- – Blood
- – Sexual contact
- – Breast milk
- – Saliva
- – Urine
- – Congenital CMV (TORCHeS infection)
- Congenital CMV
- – Most common fetal viral infection
- Clinical presentation:
- – Blueberry muffin rash: thrombocytopenia
- – Hepatosplenomegaly and jaundice
- – Sensoneural deafness
- – Intracranial calcifications: periventricular calcifications associated with toxoplasmosis
- – Ventriculomegaly
- – Mental retardation*Number 1 cause from a congenital viral infection*
- – Seizures
- More likely asymptomatic than symptomatic: 80-90% asymptomatic
- 15% progress to have sensoneural hearing loss later in life
- **2nd trimester: highest risk of infection
- Cause:
- Hydrops fetalis:
- – Heart failure leading to severe edema and fluid accumulation in multiple compartments
- – Commonly leads to spontaneous abortion
- Most common cause of sensorineural hearing loss
- Reactivation in immunosuppressed patients
- – Transplant recipient patients: at risk for developing CMV pneumonia
- – AIDS patients: CD4+ <50: Retinitis, esophagitis, colitis
- Hydrops fetalis:
- Diagnosis:
- – Owls eye inclusion bodies
- Treatment:
- – Ganciclovir
- – Phoscarnate: if resistant to ganciclovir
- Immunocompetent patients:
- – CMV mononucleosis
- Differential:
- similar to EBV mono
- Sore throat, LAD, and fatigue
- Differentiate: Mono spot test
- – Negative in CMV
- – Positive in EBV
- similar to EBV mono
Varicella Zoster virus (VZV)
- Features:
- dsDNA
- Enveloped
- Herpes virus family
- Causes:
- Chicken pox and Shingles
- Chicken pox: Childhood exanthem
- Transmission:
- – Respiratory droplets
- Clinical presentation:
- – Fever
- – Headache
- – Rash: “Dew drops on a rose” vesicular lesions on top of erythema- similar to herpes simplex virus
- Rash has different stages of healing
- Complications:
- – Adult chickenpox-> higher likelihood of developing pneumonia and encephalitis
- – Immunocompromised are more at risk
- Vaccine for Chickenpox
- – Live attenuated vaccine for children
- Treatment for chickenpox:
- – Acyclovir: for children >12, adults and immunocompromised patients
- VZV remains latent in dorsal root ganglia
- – Reactivation when stressed or immunocompromised
- – Occurs in older individuals or immunocompromised
- Reactivated VZV–> herpes zoster/shingles
- – Acyclovir: for children >12, adults and immunocompromised patients
- Clinical presentation:
- – Rash: “Dew drop on rose” appearance
- Rash travels down sensory nerve fibers of only one dermatome: typically thoracic dermatome and usually doesn’t cross midline
- – Rash is painful: postherpetic neuralgia- pain in same dermatomal distribution after rashes subsides
- – Rash: “Dew drop on rose” appearance
- Diagnosis
- – Tzank smear: multinucleated giant cells
- Vaccine:
- – Zoster vaccine: live attenuated virus
- – Recommended for adults >60
- Treatment:
- – Acyclovir
- – Famcyclovir – for shingles
- – Valacyclovir
- Congenital varicella
- – If pregnant women gets infected with VZV within first 2 trimesters, the child may develop a constellation of congenital symptoms including:
- – limb hypoplasia, cutaneous scarring in dermatomal pattern, and blindness
Roseola (HHV-6)
- Features:
- dsDNA virus: replicates in nucleus
- Herpes virus
- Primary host:
- humans
- “Sixth disease” Childhood exanthem
- Causes:
- Roseola/Exanthem subidum
- Infects CD4 helper T cells
- Clinical presentation:
- – Infects primarily children 6 months to 2 years
- – High fever lasting 3-4 days: high fevers that can cause seizures: >104F febrile seizures
- – Diffuse macular rash following high fever: lacy appearance and spares the face
- No treatment
- Supportive care:
- cooling and adequate fluids
Kaposi Sarcoma (HHV-8)
- Features:
- dsDNA: replication in nucleus
- Affects immunosuppressed patients
- Transmission:
- – Sexual contact: kissing, and men having sex with men
- Classic presentation:
- – AIDs
- – Immunocompromised
- – Elderly Russian men: lesions on lower extremities
- – Areas of Africa endemic: seen on hard palate of adults and it may be fatal in children
- Clinical presentation:
- – Erythematous, Violacious lesions on nose, extremities, and mucous membranes
- – Plaque, patch, macule, or nodule
- – Lesions rise from primitive vasculature forming mesenchymal cells
- Angiogenesis causes violaceous color
- Most common location of lesion: Hard palate
- Differential diagnosis:
- – Similar to other pathological entities
- – Bacillary angiomatosis: caused by bartonella henslae
- Definitive diagnosis:
- – Lesion examined microscopically – lymphocytic infiltrate
- Treatment:
- – Anti-retroviral therapy in HIV positive patient who has NOT been started with anti-retroviral therapy
Polyomavirus: JC and BK
- Features:
- dsDNA
- Naked
- Circular DNA
- 2 Types:
- – JC virus
- Clinical presentation:
- – Progressive multifocal leukoencephalopathy/PML
- – Demyelinating disease: kills oligodendrocytes
- – Multifocal brain lesions in white matter
- – Non-enhancing lesions
- – Progressive: patients die within a few months
- – PML is similar to MS
- – Half of population IS infected with JC virus but does not have symptoms because they are immunocompetent
- – Immunocompromised patients specifically HIV patients <200 CD4 or patients taking immunosuppressants
- Clinical presentation:
- – BK virus
- Classic presentation:
- – Nephropathy and other UTI like hemorrhagic cystitis
- Classic history:
- – Patients who have received organ transplants/kidney and bone usually obtain virus
- Classic presentation:
- – JC virus
HPV (Papillomavirus)
- Features:
- dsDNA
- Naked
- >100 papilloma virus types: only 6 are important
- Types:
- HPV 1-4
- – Skin lesions: verruca vulgaris – common wart
- – Transmission: Physical contact
- HPV 6 and 11
- – Associated with 2 diseases:
- 1. Laryngeal papillomatosis: recurrent respiratory papillomatosis- tumors/papillomas develop in airwas
- – Commonly seen in children
- – Acquired HPV 6 or 11 through vaginal birth
- 2. Anogenital warts
- – Condyloma acuminate- anogenital warts from HPV 6 and 11
- – Seen in sexually active individuals
- -Transmission: sexual
- HPV 16 and 18
- – Causes different types of anogenital squamous cell carcinomas
- – HPV 31 and 33 also causes anogenital squamous carcinomas
- – Transmission: sexual contact
- HPV 1-4
- Vaccination:
- – HPV 6, 11, 16, and 18
- – Gardasil- inactivated/killed subunit vaccine
- HPV- most common STD. Nearly all sexually active individuals obtain HPV at some point
- HPV disrupts regulation of cell cycle: HPV encodes E6 and E7 which promote proteolysis of p53 and Rb–> increasing risk of cancer
- Post coital bleeding- think cervical cancer
- Diagnosis:
- – PAP smear
- Risk factor of HPV:
- – Immunosuppression
- – HIV+
- – AIDS
Parvovirus B19
- Features:
- *Only ssDNA virus*
- Naked viurs
- Smalest DNA virus
- Causes: “Slapped cheek rash” commonly by children
- Transmission:
- – Respiratory droplets
- – Vertical: mother to baby in utero
- Clinical presentation:
- Slapped cheek disease/Fifths disease/Erythema infectiousum
- – Low grade fever lasting a week
- – After fever, “slapped cheek” rash on face
- – Lacy reticular pattern that travels down the body
- Adults disease:
- – Joint pain
- – arthritis
- – edema
- Associated with: transient aplastic anemia
- – especially in sickle cell disease
- – Transient and will fade as virus clears
- Vertical transmission:
- – Part of TORCHeS
- – Can be severe
- – First 2 trimesters–> hydrops fetalis can occur
Adenovirus
- Features:
- dsDNA
- Naked virus
- Commonly cause infection of adenoids and tonsils
- Causes: Tonsilitis
- Transmission:
- – Respiratory droplets
- – Fecal oral route
- At risk:
- – Children
- – Military recruits- close quarters
- – People who frequent public pools
- Clinical presentation:
- – Hemorrhagic cystitis: bladder infection causing hematuria
- 3 major disease process:
- – Tonsilitis
- – Hemorrhagic cystitis
- – Viral conjunctivitis
- Vaccine:
- – live vaccine only for military recruits
Poxvirus
- Features:
- dsDNA virus
- Enveloped
- Replicates in cytoplasm: DNA dependent RNA polymerase
- *Largest DNA virus*
- Dumbell shaped core
- Forms intracytoplasmic inclusion bodies in cells they infect: Type B inclusions/Guarnierni bodies
- Virus makes its own envelope
- Types of poxvirus:
- – Smallpox
- – Cowpox
- – Molluscum contagiosum
- Diagnosis:
- – Biopsy of skin lesion- type B inclusions present
Smallpox virus
- Features:
- Clinical presentation:
Cowpox
- Features:
- Clinical presentation:
- Transmission:
Molluscum Contagiosum
- Features:
- Poxvirus- largest DNA virus
- Enveloped
- dsDNA
- Clinical presentation:
- – Flesh colored, dome-shaped, umbilicated lesions
- – Spares palms and soles
- – Commonly seen in trunk, axilla, antecubital fossa, and popliteal fossa
- – Most commonly seen in children
- – In healthy adults- usually associated with STI as a single umbilicated lesion
- – Immunosuppressed patients or patients with HIV-> lesions are diffuse
Hepatitis B
- Features:
- Hepadnavirus family
- dsDNA virus: circular partially ds
- Enveloped
- Transmission:
- – Sex
- – Sharing blood products
- – Sharing needles
- – Vertical transmission
- Clinical presentation:
- – Hepatitis: UQ pain
- – Acute hepatitis
- – Chronic hepatitis: 5-10% will develop into chronic
- Newborns infected with HepB have 90% chance of developing chronic infection
- – Prodromal serum sickness of rash and arthralgias: purpuric rash with non-blanching dark macules
- – Glomerulonephritis: membranous GN- thickened membrane
- – Membranoproliferative GN- deposits in mesangium -> tram track appearance
- – Polyarteritis nodosa
- systemic vasculitis that affect medium to small arteries. Small aneurysms from the small arteries look like “beads on a string” Affects blood
- vessels leading to kidney–> reduced GFR and hypertension–> kidney damage
- Diagnosis stage of HepB:
- – Enzymes: Viral hepatitis and alcohol increase enzymes. ALT > AST Serology:
- – HBsAg: first marker of infection: if positive: active infection
- – HBeAG: second antigen to appear. Correlates with infectivity.
- – Anti-HBc: positive during window period when patient starts to develop anti-HBs Ab
- – Anti-HBe: antibody to HBeAG, low infectivity. not useful
- – Anti-HBs: if positive, indicates recovery
- Chronic hepatitis B
- – Associated with Cirrhosis and HCC
- Hepatitis D
- – Can’t cause any disease without Hepatitis B
- – RNA negative virus
- – Enveloped
- – Circular genome RNA
- – Requires HBsAg of HepB to cause infection
- 2 types of infection
- – Co-infection: both viruses transmitted simultaneously
- – Superinfection: HepD transmitted on top of existing HepB infection. Worse infection
- Treatment:
- Acute:
- – usually self limited
- Chronic and pregnant women:
- – antiviral: lamivudine
- – NRTIs
- – Interferon therapy: interferon alpha
- – Pregnant women: give medication prior to delivery
- If mother is HepB +, give newborn HepB Ig and vaccine for both passive and active immunity
- Acute: