DNA Virus


DNA Virus section provides High Yield Information needed for USMLE, COMLEX, Medical School, Residency, and as a practicing Physician.



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
  • 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
  • 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
  • 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
  • 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

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
  • 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
  • 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
    • 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

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
  • 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


Cowpox


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