PICORNAVIRIDAEEnteroviruses: polio, coxsackie, echo and hepatitis A - replicate at 37°C and stable in acid conditions
Rhinoviruses - replicate at 33°C and acid-labile
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Human Papillomavirus
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| AKA: HPV |
| Classification: Papovaviridae family, 70 genetically distinct subtypes |
| Structure: circular ds DNA virus, unenveloped, cuboidal |
| Clinical:
Benign squamous papillomas - 1, 2, 4, 7 Genital warts with low malignant potential - 6, 11, 12 Cervical squamous carcinoma - 16, 18 (31, 33, 35, 51) |
| Pathophysiology: In benign and preneoplastic lesions the genome is maintained in episomal (nonintegrated) form. Integration always occurs within the E1/E2 open reading frame of the viral genome. The E2 region represses E6/E7 transcription. E6 binds p53 and E7 binds underphosphorylated Rb. Infection acts as an initiating event. Promoted by smoking, coexisting microbial infections, dietary deficiencies, hormonal changes. |
| Micro: |
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Hepatitis
B Virus
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| AKA: HBV |
| Structure: partialy ds circular DNA, icosahedral nucleocapsid, enveloped |
| Classification: Hepadnaviridau family |
| Transmission: Blood, sexual, vertical |
| Clinical: Long incubation period 10-12 weeks; Hepatitis (jaundice, fatigue, hepatomegaly), arthralgias, immune-complex glomerulonephritis and vasculitis; high rate of hepatocellular carcinoma in chronic carriers. |
| Diagnosis: Immunoassay for HBsAg. HBeAg is an indicator of transmissibility, 10% become chronic carriers: HBsAg persists >6 mos. Order of markers: HBsAg, HBeAg/HBV DNA/DNA pol, IgM anti-HBc, Anti-HBe, IgG anti-HBs (acute infection with resolution); loss of circulating HBeAg in some mutants is associated with fulminant hepatitis. |
| Pathophysiology: Has DNA-dependent DNA polymerase; some of the DNA integrates into hepatocyte DNA. Immune attack against viral antigens on infected hepatocytes mediated by CD8+ T cells. |
| Treatment: a-IFN for chronic carriers |
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Prevention: Hepatitis B vaccine and/or Hepatitis B Ig (HBIG) [use both at separate sites following a needle-stick injury] |
| PICORNAVIRIDAE |
| Structure: Single stranded RNA with positive polarity (functions as mRNA), nonenveloped, icosahedral nucleocapsid. |
| Classification:
Enteroviruses: polio, coxsackie, echo and hepatitis A - replicate at 37°C and stable in acid conditions Rhinoviruses - replicate at 33°C and acid-labile |
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Poliovirus
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| Classification: 3 antigenic types |
| Host: primates |
| Transmission: fecal-oral; replicates in the oropharynx and intestinal tract. Virus excreted before symptomatic and for many months thereafter. |
| Structure: ss RNA, nonenveloped, icosahedral nucleocapsid |
| Clinical:
affects anterior horn and brainstem motor neurons. Infection provides lifelong
type-specific immunity. Only 1% of infections are clinically apparent. ange of responses from asymptomatic, nonparalytic poliomyelitis (aseptic meningitis) to paralytic poliomyelitis (flaccid paralysis and life-threatening respiratory paralysis). 10-14 day incubation period. A post-polio syndrome may occur many years later. |
| Treatment: Symptomatic relief and respiratory support; passive immunization with immune serum globulin in exposed, unimmunized individuals. |
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Prevention: Killed vaccine (Salk, inactivated, IPV) and live, attenuated vaccine (Sabin, oral, OPV); Livevaccine is preferred because of IgA stimulation and oral administration route. Rarely reverts to virulent strain so killed vaccine is used in immunocompromised patients and initial vaccination of an unimmunized adult. Children vaccinated at 2, 4, 6, and 18 months and booster when enters school. |
| Structure: ss RNA, nonenveloped, icosahedral nucleocapsid |
| Classification: Group A (24 serotypes) and Group B (6 serotypes) |
| Transmission: fecal-oral and respiratory aerosols |
| Clinical:
Group A cause herpangia (fever, sore throat, oopharyngeal vesicles) and hand-foot-and-mouth disease (vesicular rash on hands and feet and ulcerations in the mouth in kids - coxsackievirus A16 ). Group B cause pleurodynia, myocarditis and pericarditis; coxsackievirus B4 implicated in juvenile diabetes. Both cause non-specific URI, febrile rashes and aseptic meningitis. |
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Echovirus
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| AKA: ECHO is an acronym for enteric cytopathic human orphan |
| Structure: ss RNA, nonenveloped, icosahedral nucleocapsid |
| Classification: 30 serotypes |
| Transmission: fecal-oral |
| Clinical: leading cause of aseptic meningitis, URI, febrile illness with or without rash, infantile diarrhea, hemorrhagic conjunctivitis |
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Other Enteroviruses
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| Enterovirus 70 | acute hemorrhagic conjunctivitis |
| Enterovirus 71 | viral CNS disease (meningitis, encephalitis, paralysis) |
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Enterovirus 72 |
Hepatitis A virus |
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Hepatitis
A Virus
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| AKA: Enterovirus 72 |
| Structure: ss RNA, nonenveloped, icosahedral nucleocapsid |
| Classification: one serotype |
| Transmission: fecal-oral, rare blood-borne, shellfish consumption |
| Clinical: incubation period 2-6 weeks; does not cause chronic hepatitis or a carrier state. Clinical disease is mild or asymptomatic and rare after childhood. mortality from fulminant hepatitis 0.1%; majority resolve in 2-4 weeks. |
| Diagnosis: IgM appears at symptom onset, 50-75% of adults IgG+ |
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Prevention: Hepatitis A vaccine (formalin-inactivated virus) |
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Rhinovirus
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| AKA: cold virus (colds also caused by coronavirus, adenovirus, influenza C virus, coxsackievirus) |
| Structure: ss RNA, nonenveloped, icosahedral nucleocapsid |
| Classification: more than 100 serotypes |
| Transmission: aerosols, fomites |
| Clinical: 2-4 day incubation period; symptoms include sneezing, nasal discharge, sore throat, cough and headache; last 1 week. Immunity is a function of nasal secretory antibody. |
| Pathophysiology: Cell surface receptor is ICAM-1 |
| Micro: replicate better at 33°C; acid-labile |
| Treatment: supportive therapy |
 Rotavirus
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| Structure: segmented, ds RNA, double-layered icosahedral capsid without an envelope. virion contains an RNA-dependent RNA polymerase |
| Classification: reovirus family, 6 serotypes |
| Transmission: fecal-oral; virus replicates in the mucosal cells of the small intestine damaging the transport mechanism and leading to diarrhea. Virions exit the cell by lysing it. |
| Clinical: most common cause of gastroenteritis in young children, causes a non-bloody diarrhea with no inflammation. Immunity is IgA dependent. |
| Diagnosis: Detection of rotavirus in stool by ELISA; antibody titer |
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Yellow
Fever Virus
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| Classification: 2 distinct cycles with different reservoirs and vectors |
| Transmission:
1. monkeys in tropical Africa and South America - humans are accidental hosts 2. human urban disease transmitted by Aedes aegypti mosquito which breeds in stagnant water |
| Clinical: 3-6 day incubation, severe life-threatening jaundice and fever, headache, myalgias, photophobia, shock, GI bleeding |
| Treatment: No antiviral therapy |
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Prevention: Live attenuated virus vaccine |
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Dengue
Virus
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| Classification: 4 serotypes. |
| Transmission: Aedes aegypti mosquito in Carribean |
| Clinical: Classic Dengue ("breakbone fever") with influenza-like syndrome and severe muscle & joint pain, lymphadenopathy, rash, leukopenia; Dengue hemorrhagic fever has 10% fatality rate secondary to shock and hemorrhage |
| Pathophysiology: Hemorrhagic shock syndrome due to cross-reacting antibody at the time of a second dengue infection |
| Treatment: No vaccine or treatment available |
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Herpesviridae
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| Structure: Enveloped, icosahedral nucleocapsid, ds linear DNA |
| Classification: HHV-1 to HHV-8 |
| Clinical:
HHV-1 trigeminal ganglion - cold sores HHV-2 genital herpes HHV-3 (VZV) - chickenpox & shingles HHV-4 (EBV) - glandular fever/ infectious mononucleosis HHV-5 (CMV) - usually asymptomatic; transplacental infection HHV-6 and HHV-7 - exanthem subitum in children HHV-8 (KSHV) - Kaposi's sarcoma |
| Micro: Irregular lymphocytes in mono are T lymphs activated in an attempt to kill infected B cells. |