RNA Viruses II Flashcards

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1
Q

Rotavirus

A
  • Reovirus, dsRNA, segmented, naked icosahedron
  • disease causes severe gastroenteritis
  • profuse watery diarrhea, dehydration, maladsorption
  • affects infants and children (adults usually asymptomatic)
  • > 600,000 deaths, mostly in developing world
  • peak incidence in winter
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2
Q

Influenza Virus

A
  • Orthomyxovirus, (-) ssRNA, segmented, enveloped
  • acute respiratory illness, mainly during the winter
  • “uncomplicated”
  • upper and/or lower respiratory tract involvement
  • fever, headache, myalgia, and weakness
  • “complicated”
  • primary pneumonia caused by influenza
  • secondary bacterial pneumonia
  • mixed viral and bacterial pneumonia
  • muscle involvement: myositis (pain) and rhabdomyelitis (breakdown)
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3
Q

HIV

A

-retrovirus, + ssRNA, 2 copies (can have differences), enveloped

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4
Q

Rotavirus life cycle

A
  • attach and internalization and then breaks free of early endosome
  • genome is segmented, one gene each
  • RDRP in the virion first transcribes mRNA
  • after viral proteins are translated, new virions and genome segments are synthesized in the cytoplasm
  • virions assemble and then bud into the rough ER
  • Egress is via exocytosis (membrane vesicles carry virions out) or by cell lysis
  • virions mature in gut lumen, then infect more enterocytes or are shed in profuse diarrhea
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5
Q

Rotavirus Diagnosis, Treatment, Prevention

A
  • diagnosis: not required in most cases
  • treatment: Oral rehydration solutions
  • prevention: live attenuated vaccines- Rotarix and Rotateq
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6
Q

Influenza Life Cycle

A
  • the Haemagglutin lets it bind to the cell and endocytosis
  • it is released inside the cell, the cRNA and mRNA is made in the nucleus
  • genome is segmented, (-) ssRNA
  • genome segments traffic to the nucleus for transcription and replication by RDRP
  • viral proteins and genome segments accumulate at the plasma membrane
  • virions assemble and egress by budding
  • Neuraminidase (N antigen) releases virions from sialic acid on cell surface (antiviral target)
  • virions are shed in respiratory droplets (coughs and sneezes)
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7
Q

Flu Treatments and Prevention

A
  • Antiviral drugs
  • Tamiflu (oseltamivir), Influenza A and B
  • Relenxa (zanamirivir), Influenza A and B
  • Amantadine and Rimantadine, Influenza A only

Vaccines

  • Fluzone- trivalent inactivated vaccine
  • FluMist live attenuated vaccine

2013-2014 trivalent vaccines

  • A/California/7/2009 ) H1N1
  • A/Texas/50/2012 H3N2
  • B/ Yamagata lineage
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8
Q

Influenza Reassortment and Mutation

A
  • different subtypes of influenza A
  • there is an antigenic shift (genetic shuffling)
  • this causes a pandemic flue with a new influenza A subtype
  • there is then antigenic drift (random mutation)
  • this leads to different Influenza A strains like the seasonal flu
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9
Q

New HIV infections and AIDS related deaths

A
  • the rate of new HIV infections increased until 1996 and then has been declining gradually
  • the AIDS realted deaths increased until 2005, where there has been better medicinal control and acceptance to get treatment
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10
Q

Acute HIV Infection

A
  • Systemic: Fever, weight loss
  • Pharyngitis
  • Mouth: Sores, Thrush
  • Esophagus: Sores
  • Muscles: Myalgia
  • Liver and Spleen: Enlargement
  • Central: Malaise, Headache, Neuropathy
  • Lymph nodes: lymphadenopathy
  • Skin: rash
  • Gastric: nausea, vomiting
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11
Q

Stages of HIV Disease

A

1) Exposure to virus (transmission)
2) Primary HIV infection (acute phase)
3) Seroconversion
4) Latent period
5) Early symptomatic HIV infection
6) AIDS (CD4 cell count below 200/mm^3
7) Advanced HIV infection (CD cell count below 50/ mm^3

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12
Q

HIV Cell Tropism

A

-only humans can be infected
-virus binds to CD4 and chemokine receptors on T cells and macrophges
-depletion of these cells and chronic immune activation cause immunodeficiency
HIV-R5- co receptor is CCR5 and macrophages
HIV-R5X4- co receptor is CCR5 or CXCR4 and T cells

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13
Q

HIV Load and CD4 T cells

A
  • in the course of the HIV infection the number of CD4+ cells decreases during the acute stage but then increases again in clinical latency
  • eventually it starts to decrease gradually as the infection persists
  • the Virus load is really high in the acute infection and then is controlled and brought down when it gradually increases during the clinical latency and then increases very quickly
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14
Q

Opportunistic infections with HIV/AIDS

A
  • bacterial skin infection
  • shingles
  • thrush
  • severe athletes foot fungal
  • oral hairy leukoplakia viral
  • tuberculosis bacteria
  • then AIDS defining infections
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15
Q

Top 10 Aids defining Conditions

A
1-P. carinii pneumonia
2- esophageal candidiasis
3- wasting
4- Kaposi's sarcoma
5- Disseminated M. avium infection
6- Tuberculosis
7- Cytomegalovirus disease
8- HIV-associated dementia
9- Recurrent bacterial pneumonia
10- toxoplasmosis
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16
Q

Main symptoms of AIDs

A
  • Neurological: Encephalitis, Meningitis
  • Eyes: Retinitis
  • Lungs: Pneumocystis pneumonia, Tuberculosis (multiple organs), Tumors
  • Skin: Tumors
  • Gastrointestinal: esophagitis, chronic diarrhea
17
Q

HIV Life Cycle

A
  • after the virion fuses with the plasma membrane, the Reverse Transcriptase enzyme (RT, included in the virion) converts the (+) ssRNA genomes into dsRNA
  • the RT happens in the cytoplasm
  • the dsDNA genomes integrate into the host chromsome for life
  • HOST RNA Pol II transcribes mRNA from the integrated genome, which also serves as the genome that is packaged into new virions
  • viral proteins and 2 genomes bud from the plasma membrane
  • virion maturation occurs outside the cell when the viral protease cleaves the capsid proteins, forming the final trapezoidal shape
18
Q

HIV Diagnosis and Prevention

A

-Diagnosis:
Serologic assays for antibodies
Nucleic acid assays for viral load
-CD4 T cell count

Prevention:

  • risk avoidance
  • community awareness
  • public health measures
  • antiviral drugs (chemoprophylaxis)
19
Q

HIV treatment

A
  • ART= Antiretroviral Therapy
  • drugs must be combined to avoid resistance
  • new formulations reduce pills and doses, increase compliance
  • Atripla, Complera, Stribild
20
Q

Types of HIV drugs

A
  • Nucleoside reverse transciptase inhibitors (NRTIs)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
  • Protease inhibitors (PIs)
  • Integrase strand transfer inhibitors (INSTIs)
  • CCR5 antagonists
21
Q

Goals of HIV treatment

A
  • durable suppression of HIV viral load
  • restoration of immune function
  • prevention of HIV transmission
  • prevention of drug resistance
  • improvement in quality of life
22
Q

Hope for HIV vaccine

A
  • more is known about HIV than any other virus, but a vaccine remains elusive
  • what should it accomplish? sterilizing immunity, no progression to AIDS, no transmission