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General characteristics of Herpesvirus
Enveloped

Icosahedral capsid

dsDNA

Pleomorphic

Replicates in cell's nucleus

Encodes own DNA polymerase and Thymidine Kinase

Latency Associated Transcripts
What type of genome does Herpesvirus have?
dsDNA
What is the shape of Herpesvirus capsid?
Icosahedral
Is Herpesvirus enveloped or naked?
Enveloped
WHere does Herpesvirus replicate?
Viral dsDNA

Replicates in nucleus

Has its own DNA polymerase and thymidine kinase
What machinery is needed for Herpesvirus to replicate?
Must replicate in cell's nucleus

Encodes its own DNA polumerase and thymidine kinase

Necessary to replicate in cells where replication is not occurring (neurons)
What happens to the cell following the release of Herpesvirus?
Cell lysis

No budding involved
Latency Associated Transcripts
LAT

Viral genes that are expressed during the latency period of Herpesvirus

It maintains the latent state and helps bring virus out later
How does Herpesvirus avoid immune response?
1. Direct cell-to-cell spread, so no viremia, preventing antibody attack

2. Mimics IL-10 to suppress IFN response

3. Blocks MHC presentation preventing cell-mediated immunity by T-cells

4. Becomes latent so no viral proteins are made
How is Herpes Simplex Viruses spread?
Spread via Direct Contact

Mucosa to mucosa
or
Childbirth (HSV-2)
Which Herpes Simplex Viruses predominately gets transferred during childbirth?
HSV-2

50% mortality
45% cognitive impairments
5% normal
Where does HSV-1 present?
Associated with oral infections

But 15% cross-over of HSV-2
Where does HSV-2 present?
Associated with genital infections

But 15% cross-over of HSV-1
How does Herpes Simplex Viruses avoid Immune response?
1. Cell-to-cell spread prevents verimia and antibody detection

2. Forms syncytia to help cell-to-cell spread

3. Establishes latency in neurons
Where does HSV-1 establish latency?
Sensory Neuron (Trigeminal Ganglion)
Where does HSV-2 establish latency?
Sacral/Lumbar Neuron
What causes Herpes Simplex Virus to reactivate from latency?
Stress
immune suppression
Menstruation
UV light
Temperature changes
Where does Herpes Simplex Virus derive their envelope following replication and assembly?
Derived from nuclear membrane, not lipid bilayer
What are some clinical diseases of HSV?
Herpes Labialis

Herpes Whitlow

Eczema Herpeticum

Keratoconjunctivitis

Encephalitis

Primary Herpetic Gingivostomatitis
Herpes Labialis
Caused by HSV (mainly HSV-1)

Cold sores
Herpes Whitlow
Infection on the skin from HSV

Usually due to infection through open wound from the saliva of patients
Prevention for HSV
No vaccine

Avoid contact with lesions
Treatment for HSV
Acyclovir - Guanosine analog that targets thymidine kinase

Becomes incorporated into viral genome stopping DNA synthesis because it terminates the chain

Only active in infected cells
Acyclovir
Treatment for HSV and VZV (Varicella Zoster Virus)

Guanosine analog

Converted to GMP by thymidine kinase
Converted to GTP by cellular kinase
Becomes incorporated into viral genome
Stops DNA synthesis because new nucleotides cannot be added

CHAIN TERMINATOR

Works only on active infected cells (not latent ones)
How does Varicella Zoster Virus spread?
Spreads person-to-person by COUGHING/SNEEZING

Only Herpesvirus that transmits this way
Where does VZV remain latent?
Dorsal root ganglia
What is the clinical manifestation of VZV?
Chicken pox

Shingles
When causes VZV to reactivate from latency?
Risk of reactivation increases with age

Onset of shingles most common in immunocompromised pts
How does Cytomegalovirus (CMV) spread?
Neonate: Transplacental

Baby: Breast milk, saliva

Adult: Sex, transfusion, transplant
What is the most common cause of congenital infection?
Cytomegalovirus (CMV)
Where does Cytomegalovirus (CMV) remain latent?
Immune cells including lymphocytes and macrophages
What causes Mono?
4/5th of cases EBV

1/5th of cases CMV
What is the leading causes of death in HIV infected patients?
Cytomegalovirus (CMV)

Can cause neuropathy
What are the clinical manifestations of EBV?
Mono

Burkitt's Lymphoma

Nasopharyngeal carcinoma
What cell does EBV infect?
Infects B cells

Causes polyclonal hyperproliferation
What is the cause of Burkitt's Lymphoma?
EBV
How is EBV diagnosed?
Elevated mononuclear wbc count

Measure heterophile AB agglutination

Hairy Leukoplakia in HIV infected pts
What is the cause of Mono symptoms?
Caused by the aggressive T-cell response to the EBV infection and hyperproliferation of B-cells
Where does EBV remain latent?
In the throat and blood for life
What is the cause of Hairy Leukoplakia in HIV patients?
Re-emergence of EBV
What is the clinical manifestation of HHV-8
Kaposi Sarcoma Associated Herpesvirus

See in people with AIDS
What causes HHV-8 virulence?
It inactivates pRb (cellular anti-tumor gene)

Can lead to Kaposi Sarcoma
Pol Gene
Gene in HIV responsible for viral enzymes

Reverse Transcriptase, integrase, protease
gp120
Envelope glycoprotein

Responsible for binding to receptor/co-receptor

Causes bystander killing of uninfected cells by causing them to go through apoptosis
gp41
Envelope glycoprotein gene of HIV

Transmembrane protein that is responsible for fusion to cell membrane
Vif
HIV gene

Overcomes cellular intrinsic immunity of APOBEC3B
Gag
HIV gene

Responsible for structural proteins like Capsid
What does HIV infect?
Predominately CD4 T-cells (T-helper cells)

But can also infect Macrophages and DC
Where does most of the migration and replication of HIV occur?
Occurs in Gut Associated Lymphoid Tissue (GALT)
Where are HIV cells latent?
Latent in Resting Memory CD4- T-cells

Latency not by choice
When can you define full-blown AIDS?
<200 CD4 T-cells
or
<15% of total lymphocytes
and/or
AIDS defining illness
What is the primary screen for HIV?
ELISA assay

Tests for anti-HIV antibodies

Some false positives
What is the confirmatory test for HIV
After ELISA assay

do Western Blot
What are some Oral AIDS defining illnesses?
Candidiasis

Hairy Leukoplakia (EBV infection)

Kaposi Sarcoma (HHV-8 infection)
Reverse Transcriptase Inhibitor
Prevents RNA from being converted to DNA

Inhibits Reverse Transcriptase of HIV
Protease Inhibitor
Prevents cleavage of Gag and Pol during budding of HIV virus

Prevents maturation of the viron therefore no longer infections
Fusion Inhibitor
Prevents the fusion of HIV virion to cell membrane
Integrase inhibitor
Interferes with HIV virus to integrate its DNA molecule into chromosome
What antiviral was introduced that dramatically dropped deaths of people with HIV?
Protease inhibitors

It prevented the cleavage of Gag and Pol enzymes preventing the maturation of the HIV virion

Immature virion is not infectious
Reverse Transcriptase
RNA-dependent DNA polymerase

No proofreading activity

Error rate is great (10^-4 as compared to 10^-11 of cellular DNA polymerase)
Bystander killing of uninfected cells by HIV
Env glycoprotein gp120 causes apoptosis of cells that are not infected by virus

Reason for immunodeficiency since not many T-cells are killed
Long term non-progressors
LTNP

HIV exposed and uninfected individuals

They are associate with a particular MHC allele (Class I B57, B27) that allows them to sustain CD4 cells and maintain lower viral load.
Why is there Immune Exhaustion in HIV infection?
CD8 T-cells initial reduction of viral load

T-cells constantly replicating causing telomere shortening

Eventually run out of T-cells
CD4 because being killed by CD8 cells
and CD8 because can no longer replicate
Are all RNA tumor viruses retroviruses?
Yes
Are all retroviruses RNA tumor viruses?
No
Types of Human Retroviruses
Some are Tumor causing

HTLV-1 / HTLV-2 - can cause T-cell leukemia

HIV-1 / HIV-2 - does not cause cancer directly

Spumavirus

XMRV
Type of DNA tumor viruses
Herpesvirus (specifically EBV, HHV-8)

Papilloma virus

HBV / HCV

Adenovirus
General classification of Retrovirus
Enveloped

+ssRNA

Has viral RNA-dependent DNA polymerase called reverse transcriptase

Integrates into chromosomal DNA
Are retroviruses enveloped or naked?
Enveloped
What is the genome type for retroviruses
+ssRNA
Provirus
An integrated retroviral DNA genome
What is the function of Long Terminal repeats in retroviruses genome?
5' LTR contains promoter
3' LTR contains poly(A) function

It mediates integration of the viral genome into the chromosomal DNA
Rous Sarcoma Virus
Retroviruses found in birds

Known to transform normal cells and make them grow indefinitely causing cancer
What protein helps mediate fusion of the HIV molecule to the cell?
gp41 Transmembrane glycoprotein

Encoded in ENV segment
What protein helps mediate HIV binding to cell receptors?
gp120 Outer Docking Glycoprotein

Encoded in ENV segment
How can retroviruses cause insertional oncogenesis?
Activation of c-onc by inserting retrovirus near it

Inactivation of tumor suppressor gene by inserting retrovirus in it
General characteristics of Human Papilloma Virus
Naked

dsDNA

Icosahedral capsid

Causes genital warts and cervical cancer

Sexually transmitted

TYpes: 16, 18, 6, 11
How is HPV transmitter?
Sexual contact

Direct contact
HPV infection of cutaneous epithelium
Local infection

Causes warts
HPV infection of mucosal epithelium
Can cause cervical carcinoma
What types of HPV cause 70% of cervical cancer?
HPV 16 and 18
What type sof HPV causes 90% of genital warts
HPV 6 and 11
What HPV types are high risk?
HPV 16, 18, 6, and 11
What is the function of E6 and E7 proteins in HPV
E6 inactivates p53 tumor suppressor gene

E7 inactivates pRb tumor suppressor gene
What HPV type is most commonly associated with Oral Squamous Papilloma?
HPV Type 16
Oral Squamous Papilloma
Caused by HPV Type 16

Replicates in skin stem cells

Released from dying cells when they are shed
Gardasil
Vaccinates against all 4 types (16, 18, 6, 11)

Given before infection

Uses L1 capsid proteins to elicit a antibody response
Cervarix
Vaccinates against HPV 16 and 18

No protection against genital warts HPV 6, 11
General properties of Poliovirus
Belongs to Picornavirus family

Naked

+ssRNA

Icosahedral

Three serotypes (Poliomyelitis, Polio, infantile paralysis)

Transmitted fecal-oral route
What type of genome is poliovirus?
+ssRNA
Is poliovirus enveloped or naked?
Naked
How is poliovirus transmitted?
Fecal-oral route
What cells do poliovirus infect?
Primary site of replication is tonsols/oropharynx/peyer patches

Second infection of motor neurons
Polio Vaccines
Type types

Salk - Inactivated Polio Vaccine
-Uses formalin

Sabin - Live Attenuated Vaccine
Replicated well in gut, but not in nervous system --> but can revert to disease
General properties of Arboviruses
Belongs to family Flavivirus

Enveloped

+ssRNA

Icosahedral

Vector of transmission are arthropods

Infections caused by Yellow fever virus, west nile virus, dengue virus
What type of genome do arboviruses have?
+ssRNA virus
Are arboviruses enveloped or naked?
Enveloped
What types of viruses fall under Arboviruses?
Yellow fever virus

West Nile Virus

Dengue virus
General properties of West Nile Viruses
Falls under Arboviruses

Belongs to family Flavivirus

Enveloped

+ssRNA

Icosahedral

Vector of transmission are Ares mosquitos

BIRDS ARE THE MAJOR RESERVOIR
General properties of Dengue Virus
Falls under Arboviruses

Belongs to family Flavivirus

Enveloped

+ssRNA

Icosahedral

Vector of transmission are mosquitos

4 serotypes that USED to be localized

HUMANS ARE THE ONLY RESERVOIR
Antibody Dependent Enhancement of Infectivity
Occurs in Dengue infection

Reinfection of a second serotype results in antibodies from the first infection making the second infection worse
Jungle Sylvatic Cycle
Transmission between animal and arthropods

Humans occasionally bitten

Does not depend on humans

Used to identify west nile transmission (NOT DENGUE)
Urban Cycle
Transmission via human and arthropods

Dependent on close human contact

Used to identify Dengue and West Nile
Vaccine for Dengue
Tetravalent Dengue Vaccine

Does not exist yet but would like to make one to vaccinate against all 4 serotypes to prevent ADE
General properties of Prions
It is a misfolded version of our own protein

Induces normal cellular protein counterpart to change shape and to become a prion

Can be inherited or infectious

Very resistant to destruction

Elicit no immune response
How to inactivate a prion?
1N NaOH or undiluted bleach + autoclaving at 132*C for 4hours
General properties of Rhinovirus
Member of the Picornavirus family

Naked

RNA

Icosahedral capsid

Grows best at cool 33*C - Upper respiratory tract
Where does Rhinovirus infect?
It infects the upper respiratory tract because it is cooler
Virulence factor of Rhinovirus
It blocks IFN production, that is why there is less symptoms with a cold than the flu
Picornavirus
Family of virus that holds
Hepatovirus (Hep A Virus)
Enterovirus (Enteric and Rhino)
Poliovirus

Naked
RNA
Icosahedral capsid
Where do enteroviruses replicate?
Replicated in lymph nodes even though spread from fecal-oral route
Route of transmission for enteroviruses?
Fecal-oral route
Where does rotavirus infect?
Intestinal columnar epithelial cells
Route of transmission for rotavirus
Fecal oral route
What is the clinical manifestation of rotavirus?
Gastroenteritis
General properties of Rotavirus
Enteric virus

Enveloped (unique has 3 layers)

dsRNA

Transmitted fecal-oral

Infects intestinal columnar epi
Is the rotavirus enveloped or naked?
Enveloped

It has 3 layers to protect genome for intestinal enzymes
How does Rotavirus avoid INF response?
Transcription of dsRNA happens in the virion

ssRNA is spit out in cytoplasm

ssRNA is packaged and turned into dsRNA
Formalin
Inactivated Polio Vaccine

Only elicits a B-cell antibody response
What is the pro/con of Inactivated Vaccines?
Vaccines derived from virion

Elicits only B-cell Ab receponse

Shorter immunity (need boosters)

May require multiple injects to be immunized
What is the pro/con of Attenuated Vaccines?
Elicits a better immune response than inactivated vaccines

Elicits a B-cell AND T-cell response

Longer immune response

Can rarely revert
What are adjuvants?
Agents that stimulate the immune response to the vaccine

Ex: Aluminum salts and Oil emulsions (Squalene)
IFN-a
Helps as an antiviral against HBV and HCV (with Ribavarin)

Can also help inhibit DNA-dependent RNA synthesis

Causes alot of side effects
Enfuvirtide
AKA T-20 Fuzeon entry inhibitor

Inhibitor of Fusion

Binds to HIV envelope glycoprotein gp41

Prevents fusing of virus to cell membrane

Used as part of salvage therapy
Amantadine
Also Rimantadine

Inhibitor of Uncoating

Prevents acidification of endocytic vesicles by M2 Influenza protein ion channels

Only works for Influenza Type A
Picornavirus uncoating inhibitor
Binds to receptor binding canyon and prevents virion uncoating

Still in development
Ribavarin
Nucleoside analog

Inhibits synthesis of Guanosine nucleotides to prevent the synthesis of both DNA and RNA

Used for HCV infection (with INF-a)
Also against influenza-B, flaviviruses
Foscarnet
DNA synthesis / Reverse Transcriptase Inhibitor

Non-nucleoside analog that inhibits DNA polymerase

Used to treat Herpesvirus (following resistance to acyclovir), HIV, CMV

Renal side effects
Neuraminidase Inhibitor
Virus Release Inhibitor

Includes Zanamivir and Oseltamivir (Tamiflu)

Prevents Sialic acid from being cleaved on the surface of cells to prevent virion dumping
Tamiflu
Type of neuraminidase inhibitor that prevents sialic acid from being cleaved on the surface of cells preventing virion dumping
Raltegravir
Integrase inhibitor

Prevents HIV integrating into chromosomal DNA
Tenofovir
Topical antiviral that prevents HIV infection
Fungus characteristics
Eukaryotes

Non-motile

Cell wall of chitin

Plasma cell membrane of ergosterol

Heterotrophs

Reproduction via spores
What is main component of fungal cell walls?
Chitin
What is the main component of fungal cell membranes?
Ergosterol
What type of spores do Tricophyton Rubrum produce
Conidia

Produced at the tip or side of hypha
What type of spores do Sporangia produce
Sporangiospores
What type of spores do Coccidioides Immitis produce
Arthrospores

Thick-walled spores formed by hyphal septation
What type of spores do Candida Albicans produce
Chlamydospore - thick, double-walled,t form as enlarged
segments either within or at the tip of hyphae.
Chlamydospore
- thick, double-walled, resistant, asexual spores that form as enlarged
segments either within (intercalary) or at the tip (terminal) of hyphae.

Formed by Candida Albicans
Arthrospores
Thick-walled spores formed by hyphal septation

Formed by Coccidioides Immitis
Conidia
Produced at the tip or sides of hypha

Can be unicellular or multicelluar

Formed by tricophyton rubrum
Mycotoxicosis
Infection of a fungus that produces a toxin
Saprobe
Fungi feed off dead matter
Fungus Virulence
Grows at 37*C - body temp

Dimorphic

Production of hydrolytic enzymes

Adhesion molecules

Nutrient uptake

Resistance to oxidation
Mycoses
True fungal infection
Classified based on tissue infected, or type of pathogen
What type of fungal infections are cutaneous
Athlete's foot

Ringworm

Thrush
Amphotericin B
Antifungal Polyene Drug

Targets Ergosterol

Binds to ergosterol to create pores in plasma membrane

Treats Candida, Crytococcus, Aspergillus

Side effect: Nephrotoxicity
Nystatin
Antifungal Polyene Drug

Targets Ergosterol

Binds to ergosterol to create pores in plasma membrane

Treats Candida, Crytococcus, Aspergillus

Side effect: Nephrotoxicity
FluconAzole
Antifungal Azole drug

Targets enzyme that synthesizes Ergosterol

Inhibits ergosterol biosynthesis affecting fungal growth

Treats Candida, Cryptococcus, Coccidoides Immitis, Aspergillus
Caspofungin
Antifungal Echinocandin Drug

Targets Beta-1,3-glucan synthesis of the cell wall

Inhibits glucan synthesis to lead to abnormal cell wall

Treats Candidiasis and Aspergillosis

Cons: IV Administration
Does not work against Cryptococcus
5-Fluorocytosine (5FC)
Antifungal

Targets nucleus

Enters fungal wall through permease
Incorporates into RNA and undergoes abnormal protein synthesis
Also inhibits thymidine synthesis which blocks DNA synthesis

Treats Candida and Cryptococcus

Cons: Resistance
Inactive against Asperigillus
Pityriasis versicolor
Superficial infection caused by Malassezia spp

Round or oval hypo/hyper pigmented macules covered with thin scales

Macules hold yeast-like cells and short hyphae
General characteristics of Malassezia spp
Part of normal flora

Lipophilic

Infectious common in warm/humid climates

Causes Pityriasis versicolor superficial infection
Tinea pedis
AKA Athlete's foot

Cutaneous infection caused by Trichophyton rubrum
Trichophyton rubrum
Dermatophyte

Thrives as 25-28*C

Causes cutaneous infections like
Tinea pedia (athlete's foot)
Tinea corporis (ringworm)
Tinea cruris (jock itch)
Onychomycosis (nail infection)
Sporothrix Schenckii
Dimorphic fungus
Grows as a filamentous spore (MOLD) outside of the body and as a yeast unicellular form inside the body

Causes Sporotichosis Subcutaneous infection

Infected by direct inoculation
Histoplasma Capsulatum
Dimorphic Fungal Pathogen that Causes Histoplasmosis

Associated with Mississippi and Ohio River valley

Easily inhaled

Intracellular pathogen of macrophages
Modulates phagosome by increasing pH
Uptakes Ca and Fe
Cryptococcus neoformans
Fungal pathogen that causes cryptococcosis

Grows as yeast in soil AND humans

Virulence factors:
Polysaccharide capsule
Melanin production
Fights oxidative attack by macrophages

Infection by inhalation
Aspergillus spp
Saprophytic mold that is filamentous in soil AND lungs

Virulence factors
Thermotolerance
Conidial wall that allow adhesion to fibronectin
Melanin content
Siderophores scavenges for iron

Can elicit allergic response to fungal infections of the lung
Candida Albicans
Dimorphic Commensal fungus

Fourth causative agent of bloodstream infections

Causes thrush, candidemia (blood infection), denture stomatitis due to biofilms

Morphogenic switch from yeast to hyphae as temperature increases and added to serum

Can produce chlamydospores

Virulence factors:
Adherence
Secretion of hydrolytic enzymes
Biofilm formation
Morphogenetic switch
What immune response controls growth of fungi?
Cell mediated T-cell immunity

Humoral antibody response plays very little role
Intertrigo
Candida infection of skinfolds
Paronychia
Candida infection around nail beds
Diaper rash
Candida infection in babies
Vulvovaginitis
Candida infection

Increased risk due to antibiotics, pregnancy, diabetes, corticosteroid therapy
Thrush
AKA Pseudomembranous Candidiasis

Oral Candida infection

Clinical features:
White plaques that wipe off
Underlying mucosa is erythematous
Candida Esophagus
Candida infection of oral cavity

Clinical features:
White, removable plaques
Dysphagia
Candida Endocarditis
Candida vegetations on the valves of the heart

Plaques can embolize to the brain
How do you diagnosis Oral Candidiasis?
Periodic Acid Shift (PAS) stain to show hyphae
What drug is an M2 inhibitor?
Amantidine
Rimantidine

Prevents uncoating step in Influenza virus
Neuraminidase inhibitor
Tamiflu, zanamivir

Prevents neuraminidase from cleaving sialic acid during budding

Causes virus to clump at the cell surface reduce viral spread

Treatment for Influenza
Antivirals for Influenza
M2 Inhibitors: Amantidine prevents uncoating step

Neuraminidase inhibitors: prevents cleavage for sialic acid during budding causing clumping
Antigenic drift
Single base mutation of viral DNA moves
Antigenic shift
Mutation of viral DNA caused by reassortment
Diagnosis of Influenza virus
Hemagglutination assay
Which virus causes Infectious Hepatitis
Hep A Virus
WHich virus causes Serum heptatitis
Hep B Virus
Which Hepatitis virus is naked?
Hep A

Both B and C are enveloped
Which Hepatitis virus has a DNA genome?
Hep B

both A and C are +ssRNA
Which Hepatitis virus is ssRNA?
Hep A and C

Hep B has a DNA genome
WHich Hep virus is part of picornaviridae?
Hep A
Which Hep virus belongs to Flaviviridae?
Hep C
Which Hep virus has a fecal oral route of transmission?
Hep A

Both B and C are transfered through blood or sexual contact
Hepatocellular carcinoma
Chronic infection of Hep B can lead to cirrhosis of the liver

The chronic infection leads to chronic inflammatory responses damaging DNA in liver cells which can lead to liver cancer
Diagonisi of Chronic Hepatitis
>6mo of liver inflammation

Detected by Alanine aminotransferase (ALT) in the blood
HBV replication
Virus is a combo of ds/ssDNA

WHen it gets into cell, it finishes making the double-stranded DNA

Goes into the nucleus and makes RNA

RNA makes proteins like reverse transcriptase
AND
RNA --> DNA through reverse transcriptase

THen it packages virion
Treatment of Hep B
No antivirals
Chronic infection can be treated with RT inhibitors Lamivudine

Vaccine using HBAg particles
HBV Vaccine
Subunit vaccine

Uses recombinant DNA technology to make HBAg particles
Lamivudine
RT inhibitor

Treats HIV, chronic HBV
What transcribes dsDNA into RNA?
DNA dependent RNA polymerase
What replicates dsDNA?
DNA-dependent DNA polymerase
Replicase
Viral nucleic acid polymerase
AKA RNA-dependent RNA Polymerase

Found in Poliovirus
dsDNA Viruses
Herpes SImplex

Adenovirus

Human Papillomavirus
Does a pox virus need its own enzyme to replicate its genome?
Yes

It can replicate in the cytoplasm
Can a cell generate RNA from RNA?
No

Need reverse transcriptase or replicase
can a cell translate dsRNA?
No because it does not exist in our cells
+ssRNA Viruses
Poliovirus

Rhinovirus

Hep A, C

Yellow Fever, Dengue, West Nile
-ssRNA Viruses
Influenza

They must carry their own RNA polymerase in the virion to convert -RNA to +RNA
dsRNA Viruses
Rotavirus

Needs RNA-dependent RNA polymerase
Can a virus generate DNA from RNA?
Yes

Retroviruses only using reverse transcriptase