47. animal viruses

8/6/2019 47. Animal Viruses

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Animal Viruses

Influenza Virus H5N1 (avian influenza)

General Features of Viruses

Viruses consist of nucleic acid (DNA or RNA) surrounded by a protein coat called acapsid . The capsid is made up of individual structural subunits called capsomeres . Thecombination of the nucleic acid genome enclosed in the capsid is called thenucleocapsid . In addition, many animal viruses have an envelope , which is amembranous lipid structure that surrounds the nucleocapsid.

The structural components of a Herpes virus are illustrated below.



Herpes simplex Virus 1, illustrating the basic structural features of a virus. HSV1 is an enveloped,

icosahedral DNA virus. The region between the outer lipid envelope and the nucleocapsid is calledthe tegument. The DNA of the virus resides in the core. The envelope proteins ("GlycoproteinSpikes") are unique viral proteins, but the envelope itself is derived from the virus host cell. Viruses are quite different from cells. They contain only one type of nucleic acid, DNAor RNA, never both. They lack membranes and a cytoplasm, as well as ribosomes andany means to produce energy. Although viruses can replicate, mutate and maintaingenetic continuity, which are features of all cells, they depend entirely upon a host cell tosupply a habitat, energy, and raw materials (precursors) for viral replication. Thus,viruses must exist as obligate intracellular parasites of cells.

Viruses are very small in size. Some are not as large as a cell ribosome. Their size is sosmall that individual virus particles cannot be visualized with the light microscope. Therange of particle size is from about 20 nanometers for a small virus (e.g. poliovirus) toabout 0.3 micrometers for a very large virus (e.g. smallpox (variola) virus).

Animal viruses have many shapes ranging from cubical, bullet-shaped, polygonal,spherical, filamentous or helical, to a complex layered morphoplogy. One of the mostcommon morphologies of the viral capsid is the icosahedron , which consists of 20triangular faces (capsomeres) that coalesce to form a roughly spherical structureenclosing the viral nucleic acid. The herpes virus illustrated above has the icosahedralshape.



Common morphologies seen in animal viruses. Left to Right. A naked icosahedral virus (e.g.poliovirus), an enveloped icosahedral virus (e.g. herpes virus), a naked helical virus, and anenveloped helical virus (e.g. influenza virus). Individual capsomeres are arranged to form a capsidwhich encloses the nucleic acid (DNA or RNA) of the virus.

Classification of Viruses

The primary criteria for taxonomic classification of animal viruses are based onmorphology (size, shape, etc), type of nucleic acid (DNA, RNA, single-stranded, double-stranded, linear, circular, segmented, etc.), and occurrence of envelopes. ssRNA viruses

possess either (+)RNA (if it serves as messenger RNA) or (-)RNA (if it serves as atemplate for messenger RNA). Host range is not a particularily reliable criterion for classification. Although some animal viruses exhibit a very narrow or specific host range,such as HIV in humans or canine distemper virus (CDV) in dogs. But for classification

purposes, host range cannot be a criterion because each animal species is subject toinfection by a wide variety of viral agents, and numerous viruses infect several differentanimal species. For example, West Nile virus has a primary host of birds, but it infectsand causes disease in horses and humans. Some viruses, such as the influenza virus, areable to change their structure in such a way that they can shift from one primary host toanother, for example birds to humans.

Morphologic similarity among animal viruses correlates closely with similarity of viralcomponents, particularly with the type and size of the viral nucleic acid (genome). For example, all viruses with the morphology of adenoviruses contain dsDNA genomes witha molecular weight of about 23 million daltons; all reoviruses contain segmented dsRNAgenomes. In fact, a system of virus classification based on structure and size of viralgenomes yields that same grouping as one based on morphology. This information isorganized in two ways.

According to the Baltimore method of classification , animal viruses are be separatedinto several classes, grouped by type of nucleic acid. Class I. dsDNA viruses; Class II.ssDNA viruses; Class III. dsRNA viruses; Class IV. (+)RNA viruses; Class V. (-)RNAviruses: Class VI. RNA reverse transcribing viruses; Class VII. DNA reversetranscribing viruses. The Baltimore method of classification is illustrated in the table

below.



Baltimore Method of classification of animal viruses, grouped by genome structure. This methodclassifies viruses with regard to the various mechanisms of viral genome replication. The centraltheme is that all viruses must generate positive strand mRNAs [(+) RNA] from their genomes, inorder to produce proteins and replicate themselves. The precise mechanisms whereby this is achieveddiffer for each virus family. These various types of virus genomes can be broken down into seven

strategies for their replication. For a more complete listing of family groups of viruses classified bythe Baltimore method, please see www.virology.net/BigVirology/BVFamilyGroup.html

On the basis of morphology alone, animal viruses are organized into a heirarchal schemeconsisting of virus families and contitutive genera based on size, shape, type of nucleicacid and the presence or absence of an envelope. Some families of viruses generated inthis scheme are described and illustrated below.

http://www.virology.net/Big_Virology/BVFamilyGroup.html

http://www.virology.net/Big_Virology/BVFamilyGroup.html



Some families of Animal Viruses

Replication of Animal Viruses

Outside its host cell a virus is an intert particle. However, when it encounters a host cell it becomes a highly efficient replicating machine. After attachment and gaining entry intoits host cell, the virus subverts the biosynthetic and protein synthsizing abilities of the cell



in order to replicate the viral nucleic acid, make viral proteins and arrange its escape fromthe cell. The process occurs in several stages and differs in its details among DNA-containing and RNA-containing viruses.

The Stages of Replication

1. The first stage in viral replication is called the attachment (adsorption) stage . Like bacteriophages, animal viruses attach to host cells by means of a complementaryassociation between attachment sites on the surface of the virus and receptor sites on thehost cell surface. This accounts for specificity of viruses for their host cells. Attachmentsites on the viruses (usually called virus receptors ) are distributed over the surface of thevirus coat (capsid) or envelope, and are usually in the form of glycoproteins or proteins.Receptors on the host cell (called the host cell receptors ) are generally glycoproteinsimbedded into the cell membrane. Cells lacking receptors for a certain virus are resistantto it and cannot be infected. Attachment can be blocked by antibody molecules that bindto viral attachment sites or to host cell receptors. Since antibodies block the initial

attachment of viruses to their host cells, the presence of these antibodies in the hostorganism are the most important basis for immunization against viral infections.

2. The penetration stage follows attachment. Penetration of the virus occurs either byengulfment of the whole virus, or by fusion of the viral envelope with the cell membraneallowing only the nucleocapsid of the virus to enter the cell. Animal viruses generally donot "inject" their nucleic acid into host cells as do bacteriophages, although occassionallynon enveloped viruses leave their capsid outside the cell while the genome passes into thecell.

3. Once the nucleocapsid gains entry into the host cell cytoplasm, the process of uncoating occurs. The viral nucleic acid is released from its coat. Uncoating processesare apparently quite variable and only poorly understood. Most viruses enter the host cellin an engulfment process called receptor mediated endocytosis and actually penetrate thecell contained in a membranous structure called an endosome. Acidification of theendosome is known to cause rearrangements in the virus coat proteins which probablyallows extrusion of the viral core into the cytoplasm. Some antiviral drugs such asamantadine exert their antiviral effect my preventing uncoating of the viral nucleic acid.

4. Immediately following uncoating, the viral synthesis stage begins. Exactly how theseevents will unfold depends upon whether the infecting nucleic acid is DNA or RNA.

In DNA viruses, such as Herpes, the viral DNA is released into the nucleus of the hostcell where it is transcribed into early mRNA for transport into the cytoplasm where it istranslated into early viral proteins . The early viral proteins are concerned withreplication od the viral DNA, so they are transported back into the nucleus where they

become involved in the synthesis of multiple copies of viral DNA. These copies of theviral genome are then templates for transcription into late mRNAs which are alsotransported back into the cytoplasm for translation into late viral proteins . The late

proteins are structural proteins (e.g. coat, envelope proteins) or core proteins (certain



enzymes) which are then transported back into the nucleus for the next stage of thereplication cycle.

In the case of some RNA viruses (e.g. picornaviruses), the viral genome (RNA) stays inthe cytoplasm where it mediates its own replication and translation into viral proteins. In

other cases (e.g. orthomyxoviruses), the infectious viral RNA enters into the nucleuswhere it is replicated before transport back to the cytoplasm for translation into viral proteins.

5. Once the synthesis of the various viral components is complete, the assembly stage begins. The capsomere proteins enclose the nucleic acid to form the viral nucleocapsid.The process is called encapsidation . If the virus contains an envelope it will acquire thatenvelope and asssociated viral proteins in the next step.

6. The release stage is the final event in viral replication, and it results in the exit of themature virions from their host cell. Virus maturation and release occurs over a

considerable period of time. Some viruses are released from the cell without cell death, by egestion , whereas others are released when the cell dies and disintegrates. In the caseof enveloped viruses, the nucleocapsid acquires its final envelope from the nuclear or cellmembrane by a budding off process ( envelopment ) before egress (exit) out of the hostcell. Whenever a virus acquires a membrane envelope, it always inserts specific viral

proteins into the that envelope which become unique viral antigens and which will beused by the virus to gain entry into a new host cell.

Below are illustrated the modes of replication of two viruses that conform to this model.Herpes simplex virus (HSV) is an enveloped, double stranded DNA virus; Influenza virusis an enveloped, single stranded (-)RNA virus that contains a segmented genome.



The replication cycle of Herpes Simplex virus. 1. Specific proteins in the viral envelope attach to hostcell receptors on the cell membrane. 2. Penetration is achieved when the viral envelope fuses with thecell membrane releasing the nucleocapsid directly into the cytoplasm. 3. The virion is uncoated andthe viral DNA is transported into the nucleus. 4. In the nucleus, the viral DNA is transcribed intoearly mRNAs which are transported to the cytoplasm for the translation of early proteins. Theseearly proteins are brought back into the nucleus and participate in the replication of the virus DNAinto many copies. The viral DNA is then transcribed into the late mRNAs which exit to the cytoplasmfor translation into the late (nucleocapsid and envelope) proteins. 5. The capsid proteins encapsidatethe newly replicated genomes. The envelope proteins are imbedded in the nuclear membrane. 6. Thenucleocapsids are enveloped by budding through the nuclear membrane, and the mature viruses arereleased from the cell through cytoplasmic channels. To view an animation of the life cycle of Herpesgo to the Homepage of Dr. Edward K. Wagner at U Cal Irvine

http://darwin.bio.uci.edu/~faculty/wagner/movieindex.html





The replication cycle of Influenza A Virus. Diagram from accessexcellence.org 1. The virus adsorbsto the cell surface by means of specific receptors. 2. The virus is taken up in a membrane enclosedendosome by the process of receptor mediated endocytosis. 3. Uncoating takes place in the endosomeand the viral RNA (genome) is released into the cytoplasm. 4. The (-)RNA of the viral genome istransported into the nucleus where it is replicated and copied by a viral enzyme into (+)RNA which isboth messenger RNA and serves as a templatee for more (-)RNA. The (+)RNA is transported into thecytoplasm for translation into early and late viral proteins. 5. The viral core proteins are transportedback into the nucleus to assemble as the capsid around the viral (-)RNA forming the"ribonucleoprotein core" or the genome-containing nucleocapsid of the virus. The viral envelopeproteins assemble themselves in the cell membrane. 6. The nucleocapsid recognizes specific points oncell membrane where viral proteins have become inserted and buds off of the membrane to bereleased during enclosure in the viral envelope.

How Viruses Cause Disease

Their are several possible consequences to a cell that is infected by a virus, and ultimatelythis may determine the pathology of a disease caused by the virus.

Lytic infections result in the destruction of the host cell. Lytic infections are caused byvirulent viruses, which inherently bring about the death of the cells that they infect.

When enveloped viruses are formed by budding, the release of the viral particles may be

http://www.accessexcellence.org/RC/VL/GG/influenza.html

http://www.accessexcellence.org/RC/VL/GG/influenza.html



slow and the host cell may not be lysed. Such infections may occur over relatively long periods of time and are thus referred to as peristent infections .

Viruses may also cause latent infections . The effect of a latent infection is that there is adelay between the infection by the virus and the appearance of symptoms. Fever blisters

(cold sores) caused by herpes simplex type 1 result from a latent infection; they appear sporadically as the virus emerges from latency, usually triggered by some sort of stress inthe host.

Some animal viruses have the potential to change a cell from a normal cell into a tumor cell, the hallmark of which is to grow without restraint. This process is calledtransformation . Viruses that are able to transform normal cells into tumor cells arereferred to as oncogenic viruses and their role in causing cancer in humans will bediscussed later.

The possible effects that animal viruses may have on the cells that they infect.

The vast majority of viral infections in humans are inapparent or asymptomatic. Viral pathogenesis is the abnormal situation and it is of no particular value to the virus,although it typically results in the multiplication of the viruses that can be transmitted toother individuals. For pathogenic viruses, there are a number of critical stages inreplication which determine the nature of the disease they produce.



The Stages of Viral Infections

1. Entry into the HostThe first stage in any virus infection, irrespective of whether the virus is pathogenic or

not. In the case of pathogenic infections, the site of entry can influence the diseasesymptoms produced. Infection can occur via several portals of entry.

Skin - Most viruses which infect via the skin require a breach in the physical integrity of this effective barrier, e.g. cuts or abrasions. Some viruses employ vectors, e.g. ticks,mosquitos, etc to breach the skin.

Respiratory tract - The respiratory tract and all other mucosal surfaces possesssophisticated immune defense mechanisms, as well as non-specific inhibitorymechanisms (cilliated epithelium, mucus secretion, lower temperature, etc) which virusesmust overcome. Nonetheless, this is the most common point of entry for most viral

pathogens.Gastrointestinal tract - a fairly protected mucosal surface, but some viruses (e.g.enteroviruses, including polioviruses) enter at this site.

Genitourinary tract - less protected than the GI, but less frequently exposed toextraneous viruses.

Conjunctiva - an exposed site and relatively unprotected.

2. Primary Replication

Having gained entry to a potential host, the virus must initiate an infection by entering asusceptible cell. Some viruses remain localized after primary infection, but othersreplicate at a primary site before dissemination and spread to a secondary site. Examplesare given in the table below.

Localized Infections:

Virus: Primary Replication:

Rhinoviruses Upper respiratory tract

Rotaviruses Intestinal epithelium

Papillomaviruses Epidermis

Systemic Infections:

Virus: Primary Replication: Secondary Replication:

Enteroviruses(poliovirus) Intestinal epithelium Lymphoid tissues, CNS



Herpesvirus (HSV types1 and 2)

Oropharynx or urogenital tract

Lymphoid cells, peripheralnervous system, CNS

Rabies virus Mucle cells andconnective tissue

CNS

3. Dissemination StageThere are two main mechanisms for viral spread throughout the host: via the bloodstreamand via the nervous system.

The virus may get into the bloodstream by direct inoculation - e.g. arthropod vectors, blood transfusion or I.V. drug abuse. The virus may travel free in the plasma(Togaviruses, Enteroviruses), or in association with red cells (Orbiviruses), platelets(HSV), lymphocytes (EBV, CMV) or monocytes (Lentiviruses). the presence of virusesin the bloodstream is referred to as a viremia . Primary viremia may be followed bymore generalized secondary viremia as the virus reaches other target tissues or replicates

directly in blood cells.

In some cases, spread to nervous system is preceded by primary viremia, as above. Inother cases, spread occurs directly by contact with neurons at the primary site of infection. Once in peripheral nerves, the virus can spread to the CNS by axonal transportalong neurons (e.g. HSV). Viruses can cross synaptic junctions since these frequentlycontain virus receptors, allowing the virus to jump from one cell to another.

4. Tissue/Cell tropismTropism is the ability of a virus to replicate in particular cells or tissues. It is influenced

partly by the route of infection but largely by the interaction of a virus attachment sites

(virus receptors) with specific receptors on the surface of a cell. The interaction of thevirus receptors with the host cell receptors may have a considerable effect on pathogenesis.

5. Host Immune ResponsesThere are several ways that the host immune responses may contribute to viral pathology.The mechanisms of cell mediated immunity are designed to kill cells which are infectedwith viruses. If the mechanisms of antibody mediated immunity result in the productionof antibodies that cross-react with tissues, an autoimmune pathology may result.

6. Secondary Replication

This occurs in systemic infections when a virus reaches other tissues in which it iscapable of replication. For example, polioviruses initiate infection in the GI where the produce an asymptomatic infection. However, when disseminated to neurons in the brainand spinal cord, where the virus replicates secondarily, the serious paralytic complicationof poliomyelitis occurs. If a virus can be prevented from reaching tissues wheresecondary replication can occur, generally no disease results.

7. Direct Cell and Tissue Damage



Viruses may replicate widely throughout the body without any disease symptoms if theydo not cause significant cell damage or death. Although retroviruses (e.g. HIV) do notgenerally cause cell death, being released from the cell by budding rather than by celllysis, they cause persistent infections and may be passed vertically to offspring if theyinfect the germ line. Conversely, most other viruses, referred to as virulent viruses ,

ultimately damage or kiil their host cell by several mechanisms, including inhibition of synthesis of host cell macromolecules, damage to cell lysosomes, alterations of the cellmembrane, development of inclusion bodies, and induction of chromosomal abberations.

8. Persistence versus ClearanceThe eventual outcome of any virus infection depends on a balance between the ability of the virus to persist or remain latent (persistence) and the forces of the host to completelyeliminate the virus (clearance).

Long term persistence is the continued survival of a critical number of virus infected cellssufficient to continue the infection without killing the host. It results from two main

mechanisms:a. Regulation of lytic potential. For viruses that do not kill their host cells, this is notusually a problem. But for lytic (virulent) viruses, there may be ways to down regulatetheir replicative and lytic potential so that they can persist in a state of latency withoutreplication and damage to their host cell. This is the case with herpes viruses.

b. Evasion of immune surveillance. This may be due to several conditions that are properties of the host or the virus. Some viruses, such as influenza, can undergo antigenicshifts or antigenic drift that allows them to bypass a host immune response. Some viruses,e.g., measle, may induce a form of immune tolerance such that the host is unable toundergo an effective immune response to the virus. Other viruses, such as HIV, may setup a direct attack against cells of the immune system such that the immune system iscompromised in its ability to attack or eliminate the virus.

Appendix

1.0 The Baltimore System for Virus Classification

By convention the top strand of coding DNA written in the 5' - 3' direction is + sense.mRNA sequence is also + sense.The replication strategy of the virus depends on thenature of its genome. Viruses can be classified into seven (arbitrary) groups:

I: Double-stranded DNA (Adenoviruses; Herpesviruses; Poxviruses, etc)Some replicate in the nucleus e.g adenoviruses using cellular proteins. Poxvirusesreplicate in the cytoplasm and make their own enzymes for nucleic acid replication.

II: Single-stranded (+)sense DNA (Parvoviruses)Replication occurs in the nucleus, involving the formation of a (-)sense strand, whichserves as a template for (+)strand RNA and DNA synthesis.



III: Double-stranded RNA (Reoviruses; Birnaviruses)These viruses have segmented genomes. Each genome segment is transcribed separatelyto produce monocistronic mRNAs.

IV: Single-stranded (+)sense RNA (Picornaviruses; Togaviruses, etc)

a) Polycistronic mRNA e.g. Picornaviruses; Hepatitis A. Genome RNA = mRNA. Meansnaked RNA is infectious, no virion particle associated polymerase. Translation results inthe formation of a polyprotein product, which is subsequently cleaved to form the mature

proteins. b) Complex Transcription e.g. Togaviruses. Two or more rounds of translation arenecessary to produce the genomic RNA.

V: Single-stranded (-)sense RNA (Orthomyxoviruses, Rhabdoviruses, etc)Must have a virion particle RNA directed RNA polymerase.a) Segmented e.g. Orthomyxoviruses. First step in replication is transcription of the(-)sense RNA genome by the virion RNA-dependent RNA polymerase to produce

monocistronic mRNAs, which also serve as the template for genome replication. b) Non-segmented e.g. Rhabdoviruses. Replication occurs as above and monocistronicmRNAs are produced.

VI: Single-stranded (+)sense RNA with DNA intermediate in life-cycle (Retroviruses)Genome is (+) sense but unique among viruses in that it is diploid, and does not serve asmRNA, but as a template for reverse transcription.

VII: Double-stranded DNA with RNA intermediate (Hepadnaviruses)This group of viruses also relies on reverse transcription, but unlike the Retroviruses, thisoccurs inside the virus particle on maturation. On infection of a new cell, the first event to

occur is repair of the gapped genome, followed by transcription.1.1 List of important virus families that contain genera that infect humans and thesymptoms that they cause

DNA- containing viruses

AdenoviridaeHuman Adenoviruses - primarily respiratory and conjunctival infections

AstroviridaeAstrovirus - flulike symptoms

HerpesviridaeHerpes simplex virus type 1 - stomatitis; upper respiratory infectionsHerpes simplex virus type 2 - genital infectionsVaricella-zoster - chicken pox; herpes zoster; shingles ,Human Cyotmegalovirus - jaundice; hepatosplenomegaly, brain damage, deathEpstein-Barr Virus - Burkitt lymphoma; nasopharyngeal carcinoma; infectious



mononucleosis

PapovaviridaeHuman papilloma viruses- benign tumors (warts); cervical cancer Human polyoma viruses - progressive leukoencephalopathy (PML); transform cells

in tissue culture

PoxviridaeOrthopoxvirus

Variola - smallpoxCowpox - vesicular lesions on skin

Unclassified Round-structured virusesNorwalk agent "Noroviruses" - gastroenteritis

RNA - containing viruses

ArenaviridaeLymphcytic choriomeningitis virus (LCM) - fatal meningitisLassa virus - hemorrthagic fever, frequently fatal

BunyaviridaeHanta virus

CoronaviridaeHuman Coronavirus - SARS - severe acute respiratory syndrome

FiloviridaeEbola - acut hemorrhagic fever almost 90% case mortalityMarburg - hemorrhagic fever, frequently fatal

FlaviviridaeYellow Fever - hemorrhagic fever, hepatitis, nephritisDengue - fever, arthralgia, rashWest Nile - fever, arthralgia, rashHepatitis C virus - hepatitis

OrthomyxoviridaeInfluenza virus type A - acute respiratory diseaseInfluenza virus type B - acute respiratory diseaseInfluenza virus type C - acute respiratory disease

ParamyxoviridaeParainfluienza viruses - croup, common cold syndrome, mild respiratory diseaseMumps - parotitis, orchitis, meningoencephalitisMeasles - measles



Subacute sclerosing panencephalitis (SSPE) - chronic degeneration of CNSRespiratory syncytial virus (RSV) - pneumonia and bronchiolitis in infants and

children, common cold syndrome

Picornaviridae

Human EnterovirusesPoliovirus - poliomyelitisCoxsackie virus A - aseptic meningitis, paralysis, and common cold syndromeCoxsackie virus B - aseptic meningitis, paralysis, , severe systemic illness of

newbornsHepatitis A virus - infectious hepatitisHuman Rhinoviruses - common cold, bronchitis, croup, bronchopneumonia

ReoviridaeColorado Tick fever virus - encephalitisHuman Rotaviruses - diarrhea in infants

Retroviridae (RNA-tumor viruses)Human immunodefficiency virus - acquired immune defficiency syndroime (AIDS)Human T-lymphotrophic virus (HTLV) -

RhabdoviridaeRabies virus - encephalitis, usually fatal

TogaviridaeEastern Equine Encephalitis virus - encephalitisWestern Equine Encephalitis virus - encephalitisRubella (Measles) - severe deformities of fetuses in first trimester of pregnancy

1.2 The Big Picture Book of Viruses provide images and links and descibes viralmorphology and classification www.virology.net/Big_Virology

RNA Viruses

Picornaviridaeincludes enteroviruses, Hepatoviruses (hepatitis A), rhinoviruses, foot and-mouth diseasevirus

Togaviridaeincludes rubella

Flaviviridaeincludes "hepatitis C-type virus" and dengue

Retroviridae

http://www.virology.net/Big_Virology/BVRNApicorna.html


http://www.virology.net/Big_Virology/BVRNAtoga.html

http://www.virology.net/Big_Virology/BVRNAflavi.html

http://www.virology.net/Big_Virology/BVretro.html








Includes HIV, FLV, and MMTV

Paramyxoviridaemeasles, mumps

Rhabdoviridaerabies, vesicular stomatitis virus

Orthomyxoviridaeinfluenza

FiloviridaeMarburg and Ebola

BunyaviridaeHanta virus

ArenaviridaeIncludes lymphocytic choriomeningitisvirus

CoronavirusSARS

DNA viruses

Adenoviridaecommon cause of the common cold

Herpesviridaeincludes HSV, VZV, cytomegalovirus and Epstein-Barr Virus

Poxviridaesmallpox, variola, cowpox (Vaccinia)

Papovaviridae polyoma and human papilloma virus

HepadnaviridaeHepatitis B Virus

ParvoviridaeCanine parvovirus

Human Diseases caused by Viruses

http://www.virology.net/Big_Virology/BVRNApara.html

http://www.virology.net/Big_Virology/BVRNArhabdo.html

http://www.virology.net/Big_Virology/BVRNAortho.html

http://www.virology.net/Big_Virology/BVRNAfilo.html

http://www.virology.net/Big_Virology/BVRNAbunya.html

http://www.virology.net/Big_Virology/BVRNAarena.html

http://www.virology.net/Big_Virology/BVRNAcorona.html

http://www.virology.net/Big_Virology/BVDNAadeno.html

http://www.virology.net/Big_Virology/BVDNAherpes.html

http://www.virology.net/Big_Virology/BVDNApox.html

http://www.virology.net/Big_Virology/BVDNApapova.html

http://www.virology.net/Big_Virology/BVDNAhepadna.html

http://www.tulane.edu/~dmsander/Big_Virology/BVDNAparvo.html













http://www.tulane.edu/~dmsander/Big_Virology/BVDNAparvo.html



Acute hemorrhagic conjunctivitis - Coxsackie A-24 virus ( Picornavirus : Enterovirus),Enterovirus 70 ( Picornavirus : Enterovirus)

Acute hemorrhagic cystitis - Adenovirus 11 and 21 ( Adenovirus )

AIDS / Acquired Immune Difficiency Syndrome - human immunodeficiency virus(Retrovirus )

Bronchiolitis - Respiratory syncytial virus ( Paramyxovirus ), Parainfluenza virus(Paramyxovirus )

California encephalitis - California encephalitis virus ( Bunyavirus )

Cervical cancer - human papilloma virus ( Papovavirus )

Chickenpox - varicella zoster virus ( Herpesvirus )Colorado tick fever - Colorado tick fever virus ( Reovirus )

Conjunctivitis - Herpes Simplex Virus ( Herpesvirus )

Cowpox - vaccinia virus ( Poxvirus )

Croup, infectious - parainfluenza viruses 1-3 ( Paramyxovirus )

Dengue - dengue virus ( Flavivirus )

"Devil's grip"(pleurodynia) - Coxsackie B ( Picornavirus : Enterovirus)

Eastern equine encephalitis - EEE virus ( Togavirus )

Ebola hemorrhagic fever - Ebola virus ( Filovirus )

Gastroenteritis - Norwalk virus ( Calicivirus ), rotavirus ( Reovirus ), or various bacterialspecies

Genital HSV - Herpes Simplex Virus ( Herpesvirus )

Gingivostomatitis - HSV-1 ( Herpesvirus )

Hantavirus hemorrhagic fever / Hantaan-Korean hemorrhagic fever - Hantavirus(Bunyavirus )

Hepatitis:Hepatitis A - hepatitis A virus ( Picornavirus : Enterovirus)










http://www.virology.net/Big_Virology/BVRNAreo.html








http://www.virology.net/Big_Virology/BVRNAcalici.html































Hepatitis B - hepatitis B virus ( Hepadnavirus )Hepatitis C - hepatitis C virus ( Flavivirus )Hepatitis D - hepatitis D virus (Deltavirus)Hepatitis E - hepatitis E virus ( Calicivirus )

Herpangina - Coxsackie A ( Picornavirus : Enterovirus), Enterovirus 7 ( Picornavirus : Enterovirus)

Herpes, genital - HSV-2 ( Herpesvirus )

Herpes labialis - HSV-1 ( Herpesvirus )

Herpes, neonatal - HSV-2 ( Herpesvirus )

HIV - human immunodeficiency virus ( Retrovirus )

Infectious myocarditis - Coxsackie B1-B5 ( Picornavirus : Enterovirus)Infectious pericarditis - Coxsackie B1-B5 ( Picornavirus : Enteroviru

Influenza - Influenza viruses A, B, and C ( Orthomyxovirus )

Keratoconjunctivitis - Adenovirus ( Adenovirus ), HSV-1 ( Herpesvirus )

Lassa hemorrhagic fever - Lassavirus ( Arenavirus )

Marburg hemorrhagic fever - Marburg virus ( Filovirus )

Measles - rubeola virus ( Paramyxovirus )

Meningitis, aseptic - Coxsackie A and B ( Picornavirus : Enterovirus), Echovirus(Picornavirus : Enterovirus), lymphocytic choriomeningitis virus ( Arenavirus ), HSV-2(Herpesvirus )

Mononucleosis - Epstein-Barr virus ( Herpesvirus )

Mumps - mumps virus ( Paramyxovirus )

Pharyngitis:Respiratory Synytial Virus ( Paramyxovirus : Pneumovirus)Influenza Virus ( Orthomyxovirus )Parainfluenza Virus ( Paramyxovirus )Adenovirus ( Adenovirus )Epstein-Barr Virus ( Herpesvirus )

Pleurodynia - Coxsackie B ( Picornavirus : Enterovirus)






























































Pneumonia, viral - respiratory syncytial virus ( Paramyxovirus ), CMV ( Herpesvirus )

Polio, Poliomyelitis - Poliovirus ( Picornavirus : Enterovirus)

Progressive multifocal leukencephalopathy - JC virus ( Papovavirus )

Rabies - rabies virus ( Rhabdovirus )

Roseola - HHV-6 ( Herpesvirus )

Rubella - rubivirus ( Togavirus )

Severe Acute Respiratory Syndrome (SARS) - a human coronavirus ( Coronavirus )

Shingles (zoster) - varicella zoster virus ( Herpesvirus )

Smallpox - variola virus ( Poxvirus )

Urethritis - Herpes Simples Virus ( Herpesvirus )

Varicella - varicella zoster virus ( Herpesvirus )

Western equine encephalitis - WEE virus ( Togavirus )

Yellow fever - Yellow fever virus ( Flavivirus )

Zoster - varicella zoster virus ( Herpesvirus )































47. animal viruses

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