Virology-RNA Viruses Flashcards

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1
Q

Flaviviruses

A

Envelope
SS
Capsid icosahedral

Diseases:

  • Yellow fever
  • Dengue
  • west nilo virus
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2
Q

Yellow fever

A

Flavivirus transmitted by aedes mosquitoes.

Symptoms: fever, black vomitus and jaundice.

Councilman bodies on liver biopsy

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3
Q

Rotavirus

A

1 cause of fatal diarrhea in children (infantile gastroenteritis)

No envelope, DS linear, icosahedral capsid

Prevention: vaccine

Symptoms: anorexia, low grade fever, watery diarrhea , vomiting, abdominal cramps.

Complications: dehydration

Management: no antibiotics, only supportive

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4
Q

Rhinovirus

A

Picornavirus. Nonenvelope RNA virus
Incidence in fall and spring

Cause of common cold: low fever, sneezing, runny nose, nasal congestion, cough , headaches, sore throat.

Complications: sinusitis, otitis media, chronic bronchitis

Treatment: symptomatic management

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5
Q

Influenza virus

A

Orthomyxoviruses. Enveloped SSRNA
*Types : Influenza A or B
*Disease: influenza
-headache, malaise, fever, chills, myalgias, anorexia, bronchiolitis, croup (cough), vomiting.
*Complications: Can lead to Reye syndrome or Guillain-Barré syndrome
*Transmission: direct contact, respiratory.
*Dx: rapid test, culture and clinical symptoms
*Treatment: amantadine or zanamivir/oseltamivir
*Prevention: killed vaccine, injection.
*Pathogenesis:
Envelope contains two glycoproteins: H (hemagglutinin) and N (neuraminidase)

Two process:

  • antigenic shift :
    Sudden and major change in the surface of a virus due to a process call Genetic reassortment : two viruses which infect simultaneously the cell mix and match their genome.
    Cause pandemics: Production of a new agent to which population has no immunity.
  • Antigenic drift:
    Slight changes in antigenicity due to random mutations in H and/or N genes.
    Cause epidemics

Sudden shift
Gradual drift

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6
Q

Rubella virus

A

Togavirus. German measles

Rubella symptoms: fever, postauricular and other lymphadenopathy , arthralgias, confluent Maculopapular rash that starts on face and spreads centrifugally to involve trunk and extremities.

CONGENITAL RUBELLA (TORCHES)

  • Patent ductus arterioso, pulmonary stenosis, cataracts, microcephaly, deafness. Blueberry muffin appearance due to dermal extra medullary hematopoiesis.
  • The effects are more serious if the maternal infection is acquired during the first 16 weeks.
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7
Q

PaRaMyxovirus

A

Envelope. SS negative linear

Parainfluenza: croup

Mumps

Measles

RSV

All contains surface F protein wich cause respiratory epithelial cells to fuse and form multinucleated cells

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8
Q

Croup

Acute laryngotracheobronchitis

A

Seal-like barking cough and inspiratory stridor

Narrowing of upper trachea and sub glottis leads to characteristic steeple sign on x Ray .

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9
Q

Measles (rubeola) virus

A

Prodromal fever with cough , coryza and conjunctivitis
Eventually, koplik spots (bright red spots with blue-white center on Buccal mucosa

Followed 1-2 days later by a Maculopapular rash that starts at the head /neck and spreads downward .

3 C of measles: Cough, Coryza, Conjunctivitis

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10
Q

Mumps virus

A

*Symptoms:
PAROTITIS

ORCHITIS: can cause sterility (specially after puberty)

ASEPTIC MENINGITIS

PANCREATITIS

  • Management:supportive care
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11
Q

Ebola virus

A

Filovirus

Cell target: endothelial cells, phagocytes, hepatocytes

Incubation time : 21 days

Symptoms: abrupt onset of flu like symptoms, diarrhea, vomiting, high fever, myalgias,

Transmission: direct contact with body fluids, fomites .

Diagnose: PCR within 48 hrs of symptom onset.

High mortality rate

Treatment: supportive care , strict isolation of infected individuals.

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12
Q

Hepatitis A virus

A

Family: Picornavirus
Features: iscosahedral, Nonenvelope virus
Transmission: fecal-oral

Incubation: weeks (short)

Clinical course : *Asymptomatic
*Acute : fever, jaundice, ALT AST high, hepatomegaly

Prognosis: good

Liver biopsy: hepatocytes swelling, monocytes infiltration, councilman bodies.

No carrier state

Dx: serologic markers: IgM and IgG
Prevention: vaccine

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13
Q

Hepatitis B virus

A

Family: DNA hepadnavirus

Transmission: parenteral, sexual, perinatal

Incubation: long (months)

Clinical course: initially like a serum sickness: fever, arthralgias, rash

Prognosis 50% good resolution, 50% chronic infection

Carrier state common.

Liver biopsy: granular eosinophilic ground class appearance .

Dx: serologic markers: HBsAg, Anti-HBs, HBcAg, Anti-HBc, HBeAg, Anti-HBe

Tx:
The primary treatment goals for patients with hepatitis B infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, or hepatocellular carcinoma (HCC).[2] Pegylated interferon alfa (PEG-IFN-a), entecavir, and tenofovir disoproxil fumarate are the first-line agents in the treatment of hepatitis B disease.

Complication: chronic infection: carcinoma hepatocellular and /or cirrhosis

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14
Q

Hepatitis B serologic markers

A

Hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) (marker of infectivity) are the first markers that can be identified in the serum in acute disease. Hepatitis B core antibody (anti-HBc) immunoglobulin M (IgM) follows.

For patients who recover, seroconversion to hepatitis B surface antibody (anti-HBs) and hepatitis B e antibody (anti-HBe) is observed. The anti-HBc is of the IgG class. Patients with persistent HBsAg lasting more than 6 months are considered to have chronic hepatitis.

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15
Q

Acute hepatitis B

A

Serology markers positive:

  • HBsAg : antigen found on surface of HBV.
  • HBeAg: indicates active viral replication and therefore high transmissibility
  • Anti-HBc: IgM (anticuerpo al antigeno Del core)
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16
Q

Window period of HBV

A

Positive Anti- HBe

Indicates low transmissibility

Antibody to HBeAg

17
Q

Serology marker for a chronic HBV

A

-Low infectivity

Pos HBsAg , Pos Anti-HBe, IgG Anti-HB

  • High infectivity

Pos HBsAg, Pos HBeAg, Anti-HBc IgG

18
Q

Recovery serology markers for HBV

A
  • Anti-HBs: Antibody to HBsAg (inmunity to HB)
  • Anti-HBe
  • Anti- HBc IgG
19
Q

Immunized to HB

A

Anti - HBs

20
Q

Hepatitis C virus

A

Family RNA Flavivirus

Transmission primary blood (tattooing, drugs abusers), sexually transmitted

Incubation: long

Clinical course: May progress to cirrhosis (portal hypertension) or Carcinoma. Initial symptoms of hepatitis C are often extrahepatic, most commonly involving the joints, muscle, and skin.

Prognosis chronic hepatitis

Hepatocarinoma risk: high

Carrier state common

Diagnosis: blood test (hepatic panel) , screening for STD, serology test for hep C, in advance cases liver biopsy.

21
Q

Hepatitis D virus

A

RNA deltavirus

Transmission: parenteral, sexual, perinatal

Incubation: coinfection with HB = long, superinfection (alone)= short

Clinical course similar to HB

Prognosis of superinfection is worse than coinfection

Risk of HCC

note: defective virus, depends of HB

22
Q

Hepatitis E virus

A

RNA herpevirus

Transmission: fecal-oral, waterbone

Incubation short

Clinical course: typically self-limited, similar to hepatitis A. Could cause Fulminant hepatitis in expectant women.

The incubation period ranges from 15-60 days. The course of infection has 2 phases, the prodromal phase and the icteric phase. The prodromal phase usually is of short duration.

High mortality in pregnant women

No HCC risk

liver biopsy: patchy necrosis

Treatment: Therapy should be predominantly preventive, relying on clean drinking water, good sanitation, and proper personal hygiene. A successful recombinant hepatitis E vaccine has been developed.[

Prodromal phase symptoms:

  • Myalgias
  • Artharlgias
  • Fever
  • Anorexia
  • right upper cuadrant abdominal pain

Icteric phase

  • jaundice
  • colorless stools
  • dark urine
  • pruritus