Bacteriology at UW-Madison
The Microbial World
Lectures in Microbiology by Kenneth Todar PhD University of Wisconsin-Madison Department of Bacteriology
Animal Viruses with emphasis on pathogens of humans
© 2009 Kenneth Todar PhD
Virus H5N1 (avian influenza)
Features of Viruses
Viruses consist of nucleic acid (DNA or RNA) surrounded by a protein
coat called a capsid. The
capsid is made up of individual structural subunits called capsomeres. The combination of the
nucleic acid genome enclosed in the capsid is called the nucleocapsid. In addition,
viruses have an envelope,
which is a membranous lipid structure that surrounds the
The structural components of a Herpes virus are illustrated below.
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 called the tegument. The
DNA of the virus resides in the core. The envelope proteins
("Glycoprotein Spikes") 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, DNA or RNA, never both. They lack membranes and a
cytoplasm, as well as ribosomes and any means to produce energy.
Although viruses can replicate, mutate and maintain genetic continuity,
which are features of all cells, they depend entirely upon a host cell
supply a habitat, energy and raw materials (precursors) for viral
replication. Thus, viruses
must exist as obligate intracellular
parasites of cells.
are very small in size. Some are not as large as a cell ribosome. Their
size is so small that individual virus particles cannot be visualized
with the light microscope. The range of particle size is from about 20
nanometers for a small virus (e.g. poliovirus) to about 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
of the most common morphologies of the viral capsid is the icosahedron, which consists of 20
triangular faces (capsomeres) that coalesce to form a roughly spherical
structure enclosing the viral nucleic acid. The herpes virus
illustrated above has the icosahedral shape.
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 an enveloped helical virus (e.g. influenza virus). Individual
capsomeres are arranged to form a capsid which encloses the nucleic
acid (DNA or RNA) of the virus.
The primary criteria for taxonomic classification of animal viruses are
based on morphology (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 a template for messenger RNA). Host
range is not a
particularly 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 to infection by a wide variety of viral
agents, and numerous viruses infect several different animal species.
For example, West Nile virus has a primary host of birds, but it
infects and causes disease in horses and humans. Some viruses, such as
the influenza virus, are able to change their structure in such a way
that they can shift from one primary host to another, for example birds
Morphologic similarity among animal viruses correlates closely with
similarity of viral components, particularly with the type and size of
the viral nucleic acid (genome). For example, all viruses with the
morphology of adenoviruses contain dsDNA genomes with a molecular
weight of about 23 million daltons; all reoviruses contain segmented
dsRNA genomes. In fact, a system of virus classification based on
structure and size of viral genomes yields that same grouping as one
based on morphology. This information is organized in two ways.
According to the Baltimore method of
classification, animal viruses are
be separated into 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. (-)RNA viruses: Class
VI. RNA reverse transcribing viruses; Class VII. DNA
reverse transcribing viruses. The Baltimore method
of classification is illustrated in the table below.
Method of classification of animal viruses, grouped by genome
This method classifies viruses with regard to the various mechanisms of
viral genome replication. The central theme is that all viruses must
generate positive strand mRNAs [(+) RNA] from their genomes, in order
to produce proteins and replicate themselves. The precise mechanisms
whereby this is achieved differ 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 by the Baltimore method, please see www.virology.net/BigVirology/BVFamilyGroup.html
On the basis of morphology alone, animal viruses are organized into a
hierarchical scheme consisting of virus families and constitutive
based on size, shape, type of nucleic acid and the presence or absence
of an envelope. Some families of viruses generated in this scheme are
described and illustrated below.
families of Animal Viruses
Outside its host cell a virus is an inert particle. However, when it
encounters a host cell it becomes a highly efficient replicating
machine. After attachment and gaining entry into its host cell, the
virus subverts the biosynthetic and protein synthesizing abilities of
the cell in order to replicate the viral nucleic acid, make viral
proteins and arrange its escape from the cell. The process occurs in
several stages and differs in its details among DNA-containing and
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
complementary association between attachment sites on the surface of
the virus and receptor sites on the host cell surface. This accounts
for specificity of viruses for their host cells. Attachment sites on
the viruses (usually called virus
receptors) are distributed over
the surface of the virus 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 glycoproteins imbedded into
the cell membrane. Cells lacking receptors for a certain virus are
resistant to it and cannot be infected. Attachment can be blocked by
antibody molecules that bind to 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 host organism
are the most important basis for immunization against viral infections.
2. The penetration stage
follows attachment. Penetration of the virus occurs either by
engulfment of the whole virus, or by fusion of the viral envelope with
the cell membrane allowing only the nucleocapsid of the virus to enter
cell. Animal viruses generally do not "inject" their nucleic acid into
host cells as do bacteriophages, although occasionally non enveloped
viruses leave their capsid outside the cell while the genome passes
into the cell.
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 processes
are apparently quite variable and only poorly understood. Most viruses
enter the host cell in an engulfment process called receptor mediated
endocytosis and actually penetrate the cell contained in a membranous
structure called an endosome. Acidification of the endosome is known to
cause rearrangements in the virus coat proteins which probably allows
extrusion of the viral core into the cytoplasm. Some antiviral
drugs such as amantadine exert their antiviral effect my preventing
uncoating of the viral nucleic acid.
4. Immediately following uncoating, the viral
synthesis stage begins. Exactly how these events 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 host cell where it is transcribed into early mRNA for
transport into the cytoplasm where it is translated into early viral proteins. The early
viral proteins are concerned with replication 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 the
viral genome are then templates for transcription into late mRNAs which
are also transported 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 the replication cycle.
In the case of some RNA viruses (e.g. picornaviruses), the viral genome
(RNA) stays in the 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 nucleus
where 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 that envelope
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 the mature 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
when the cell dies and disintegrates. In the case of enveloped viruses,
the nucleocapsid acquires its final envelope from the nuclear or cell
membrane by a budding off process (envelopment)
before egress (exit) out of
cell. 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 be used by the virus to gain entry into a
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 virus is an enveloped, single
stranded (-)RNA virus that contains a segmented genome.
replication cycle of Herpes Simplex virus. 1. Specific proteins in the
viral envelope attach to host cell receptors on the cell membrane. 2.
Penetration is achieved when the viral envelope fuses with the cell
membrane releasing the nucleocapsid directly into the cytoplasm. 3. The
virion is uncoated and the viral DNA is transported into the nucleus.
4. In the nucleus, the viral DNA is transcribed into early mRNAs which
are transported to the cytoplasm for the translation of early proteins.
These early proteins are brought back into the nucleus and participate
in the replication of the virus DNA into many copies. The viral DNA is
then transcribed into the late mRNAs which exit to the cytoplasm for
translation into the late (nucleocapsid and envelope) proteins. 5. The
capsid proteins encapsidate the newly replicated genomes. The envelope
proteins are imbedded in the nuclear membrane. 6. The nucleocapsids are
enveloped by budding through the nuclear membrane, and the mature
viruses are released from the cell through cytoplasmic channels. To
an animation of the life cycle of Herpes go to the Homepage
of Dr. Edward K. Wagner at U Cal Irvine
replication cycle of Influenza A Virus. Diagram from accessexcellence.org 1.
The virus adsorbs to the cell surface by means of specific receptors.
2. The virus is taken up in a membrane enclosed endosome by the process
of receptor mediated endocytosis. 3. Uncoating takes place in the
endosome and the viral RNA (genome) is released into the cytoplasm. 4.
The (-)RNA of the viral genome is transported into the nucleus where it
is replicated and copied by a viral enzyme into (+)RNA which is both
messenger RNA and serves as a template for more (-)RNA. The (+)RNA is
transported into the cytoplasm for translation into early and late
viral proteins. 5. The viral core proteins are transported back 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
envelope proteins assemble themselves in the cell membrane. 6. The
nucleocapsid recognizes specific points on cell membrane where viral
proteins have become inserted and buds off of the membrane to be
released during enclosure in the viral envelope.
Their are several possible consequences to a cell that is infected by a
virus, and ultimately this 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 by virulent
viruses, which inherently bring about the death of the cells that they
When enveloped viruses are formed by budding, the release of the viral
particles may be 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 persistent infections.
Viruses may also cause latent
infections. The effect of a latent infection is that there is a
delay 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 in the 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 called transformation.
Viruses that are able to transform normal cells into tumor cells are
referred to as oncogenic viruses
and their role in causing cancer in humans will be discussed later.
possible effects that animal viruses may have on the cells that they
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 to other
individuals. For pathogenic viruses, there are a number of critical
replication which determine the nature of the disease they produce.
The Stages of Viral Infections
1. Entry into the Host
The 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 disease symptoms produced. Infection
can occur via several portals of entry.
Skin - Most viruses which infect via the skin require a breach
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 possess sophisticated
immune defense mechanisms, as well as non-specific inhibitory
mechanisms (ciliated epithelium, mucus secretion, lower temperature,
which viruses must 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
Genitourinary tract - less protected than the GI tract, but less
frequently exposed to extraneous 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 a susceptible cell. Some viruses remain localized
after primary infection, but others replicate at a primary site before
dissemination and spread to a secondary site. Examples are given in the
||Upper respiratory tract
||Lymphoid tissues, CNS
|Herpesvirus (HSV types 1 and 2)
|Oropharynx or urogenital tract
||Lymphoid cells, peripheral nervous system, CNS
|Muscle cells and connective
3. Dissemination Stage
There are two main mechanisms for viral spread throughout the host: via
the bloodstream and 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 viruses in the
bloodstream is referred to as a viremia.
Primary viremia may be followed
more 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. In other 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 transport
along neurons (e.g. HSV). Viruses can cross synaptic junctions
since these frequently contain virus receptors, allowing the virus to
jump from one cell to another.
4. Tissue/Cell tropism
Tropism is the ability of a virus to replicate in particular cells or
tissues. It is influenced partly by the route of infection but largely
the interaction of a virus attachment sites (virus receptors) with
receptors on the surface of a cell. The interaction of the virus
receptors with the host cell receptors may have a considerable effect
5. Host Immune Responses
There 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 infected with viruses. If the mechanisms of
antibody mediated immunity result in the production of 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
which it is capable of replication. For example, polioviruses initiate
infection in the GI where the produce an asymptomatic infection.
However, when disseminated to
neurons in the brain and spinal cord, where the virus replicates
secondarily, the serious paralytic complication of poliomyelitis
occurs. If a virus can be prevented from reaching
tissues where secondary replication can occur, generally no disease
7. Direct Cell and Tissue Damage
Viruses may replicate widely throughout the body without any disease
symptoms if they do not cause significant cell damage or death.
Although retroviruses (e.g. HIV) do not generally cause cell death,
being released from the
cell by budding rather than by cell lysis, they cause persistent
infections and may be passed vertically to offspring if they infect
the germ line.
Conversely, most other viruses, referred to as virulent viruses, ultimately damage
or kill their host cell by several mechanisms, including inhibition of
synthesis of host cell macromolecules, damage to cell lysosomes,
alterations of the cell membrane, development of inclusion bodies, and
induction of chromosomal aberrations.
8. Persistence versus Clearance
The 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 completely eliminate the
Long term persistence is the continued survival of a critical number of
virus infected cells sufficient 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 not usually a problem. But for lytic (virulent)
viruses, there may be ways to down regulate their replicative and lytic
potential so that they can persist in a state of latency without
replication and damage to their host cell. This is the case with herpes
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 antigenic shifts or antigenic drift that
allows them to bypass a host immune response. Some viruses, e.g.,
measles, may induce a form of immune tolerance such that the host is
unable to undergo an effective immune response to the virus. Other
viruses, such as HIV, may set up a direct attack against cells of the
immune system such that the immune system is compromised in its ability
to attack or eliminate the virus.
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 the nature of its genome. Viruses can
be classified into seven (arbitrary) groups:
I: Double-stranded DNA (Adenoviruses; Herpesviruses; Poxviruses,
Some replicate in the nucleus e.g. adenoviruses using cellular
Poxviruses replicate 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, which serves as a template for (+)strand RNA and DNA
III: Double-stranded RNA
These viruses have segmented genomes. Each genome segment is
transcribed separately to produce monocistronic mRNAs.
IV: Single-stranded (+)sense RNA (Picornaviruses;
a) Polycistronic mRNA e.g. Picornaviruses; Hepatitis A. Genome RNA =
mRNA. Means naked RNA is infectious, no virion particle associated
polymerase. Translation results in the 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 are necessary to produce the genomic RNA.
V: Single-stranded (-)sense RNA (Orthomyxoviruses,
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
monocistronic mRNAs are produced.
VI: Single-stranded (+)sense RNA with DNA intermediate in
Genome is (+) sense but unique among viruses in that it is diploid, and
does not serve as mRNA, but as a template for reverse transcription.
VII: Double-stranded DNA with RNA intermediate
DNA- containing viruses
This group of viruses also relies on reverse transcription, but unlike
the Retroviruses, this occurs 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.
List of important virus families that contain genera that infect humans
and the symptoms that they cause
Human Adenoviruses - primarily
respiratory and conjunctival infections
Herpes simplex virus type 1 -
stomatitis; upper respiratory infections
Herpes simplex virus type 2 -
Varicella-zoster - chicken pox;
herpes zoster; shingles ,
Human Cyotmegalovirus - jaundice;
hepatosplenomegaly, brain damage, death
Epstein-Barr Virus - Burkitt's
lymphoma; nasopharyngeal carcinoma; infectious mononucleosis
Human papilloma viruses- benign
tumors (warts); cervical cancer
Human polyoma viruses -
progressive leukoencephalopathy (PML); transform cells in tissue culture
Variola - smallpox
Cowpox - vesicular lesions on skin
RNA - containing viruses
(LCM) - fatal meningitis
Lassa virus - hemorrhagic fever,
Astrovirus - flulike symptoms
Human Coronavirus - SARS - severe
acute respiratory syndrome
Includes Small Round-structured Viruses (SRSV) such as Norwalk agent "Noroviruses" - gastroenteritis
Human Coronavirus - SARS - severe
acute respiratory syndrome
Ebola - acute hemorrhagic fever
almost 90% case mortality
Marburg - hemorrhagic fever,
Yellow Fever - hemorrhagic fever,
Dengue - fever, arthralgia, rash
West Nile - fever, arthralgia,
Hepatitis C virus - hepatitis
Influenza virus type A - acute
Influenza virus type B - acute
Influenza virus type C - acute
Parainfluenza viruses - croup,
common cold syndrome, mild respiratory disease
Mumps - parotitis, orchitis,
Measles - measles
panencephalitis (SSPE) - chronic degeneration of CNS
Respiratory syncytial virus (RSV)
- pneumonia and bronchiolitis in infants and children, common cold
Poliovirus - poliomyelitis
Coxsackie virus A - aseptic meningitis, paralysis,
and common cold syndrome
Coxsackie virus B - aseptic meningitis, paralysis,
severe systemic illness of newborns
Hepatitis A virus - infectious hepatitis
Human Rhinoviruses - common cold, bronchitis, croup,
Colorado Tick fever virus -
Human Rotaviruses - diarrhea in
Retroviridae (RNA-tumor viruses)
Human immunodeficiency virus -
acquired immune deficiency syndrome (AIDS)
Human T-lymphotrophic virus
Rabies virus - encephalitis,
Eastern Equine Encephalitis virus
Western Equine Encephalitis virus
Rubella (Measles) - severe
deformities of fetuses in first trimester of pregnancy
Big Picture Book of Viruses provide images and links and
describes viral morphology and classification www.virology.net/Big_Virology
includes enteroviruses, Hepatoviruses (hepatitis A), rhinoviruses, foot
and-mouth disease virus
includes "hepatitis C-type virus" and dengue
Includes HIV, FLV, and MMTV
rabies, vesicular stomatitis virus
Marburg and Ebola
Includes lymphocytic choriomeningitis virus
common cause of the common cold
includes HSV, VZV, Cyotmegalovirus and Epstein-Barr Virus
smallpox, variola, cowpox (Vaccinia)
polyoma and human papilloma virus
Hepatitis B Virus
Diseases caused by Viruses
Acute hemorrhagic conjunctivitis -
Coxsackie A-24 virus (Picornavirus:
Enterovirus), Enterovirus 70 (Picornavirus:
Acute hemorrhagic cystitis - Adenovirus 11 and
AIDS / Acquired Immune Deficiency 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:
Eastern equine encephalitis - EEE virus (Togavirus)
Ebola hemorrhagic fever - Ebola virus (Filovirus)
Gastroenteritis - Norwalk virus (Calicivirus),
or various bacterial species
Genital HSV - Herpes Simplex Virus (Herpesvirus)
Gingivostomatitis - HSV-1 (Herpesvirus)
Hantavirus hemorrhagic fever / Hantaan-Korean hemorrhagic fever -
Hepatitis A - hepatitis A virus (Picornavirus:
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:
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:
Infectious pericarditis - Coxsackie B1-B5 (Picornavirus:
Influenza - Influenza viruses A, B, and C (Orthomyxovirus)
Keratoconjunctivitis - Adenovirus (Adenovirus),
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),
Mononucleosis - Epstein-Barr virus (Herpesvirus)
Mumps - mumps virus (Paramyxovirus)
Respiratory Syncytial Virus (Paramyxovirus:
Influenza Virus (Orthomyxovirus)
Parainfluenza Virus (Paramyxovirus)
Epstein-Barr Virus (Herpesvirus)
Pleurodynia - Coxsackie B (Picornavirus:
Pneumonia, viral - respiratory syncytial virus (Paramyxovirus),
Polio, Poliomyelitis - Poliovirus (Picornavirus:
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)
Written and Edited by Kenneth Todar. All rights
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