VIRAL TAXONOMYVIRAL TAXONOMY18 GROUPS - 6 are DNA VIRUSES, 11 are RNA VIRUSES and 1 UNCLASSIFIED

 

DNA VIRUSESDNA VIRUSES1. Poxvirus1. Poxvirus (1) the largest viruses (2) enveloped double stranded DNA viruses (3) intracytoplasmic inclusion bodies (4) skin is a primary target (5) eg. smallpox, cowpox, vaccinia 2. Herpesvirus2. Herpesvirus (1) medium size (2) enveloped Double-stranded DNA viruses (3) intranuclear inclusion bodies (4) skin is the major target. (5) eg. chicken pox, Epstein Bar viruses

3. Adenoviurs3. Adenoviurs (1) medium size (2) Double stranded DNA viruses (3) intranuclear inclusion bodies (4) target: human lymphoid tissue. (5) eg. tumors in animals

 4. Papovavirus4. Papovavirus (1) small size (2) non-enveloped double stranded circular DNA (3) tumor producing viruses

(4) eg. papilloma virus of human, polyoma viruses of mice.

5. Parvovirus5. Parvovirus (1) ultra small in size (2) single stranded DNA viruses (3) adeno-associated viruses (4) eg. human parvovirus B19 or fifth disease 6. Hepadnavirus6. Hepadnavirus (1) enveloped DNA virus, Double stranded with single stranded region (2) replication in liver cell (3) eg. hepatitis B

RNA VIRUSESRNA VIRUSES 

7. Myxovirus (Orthomyxoviruses)7. Myxovirus (Orthomyxoviruses) (1) medium size (2) enveloped single stranded RNA virus with segmented genome and helical symmetry (3) many can agglutinate red blood cells (4) eg. influenza viruses cause flu 8. Paramyxovirus8. Paramyxovirus (1) medium size (2) enveloped single stranded RNA viruses helical symmetry not segmented (3) both intracytoplasmic and intranuclear inclusion bodies (4) eg. measles, mumps

* ARBOVIRUSES (Arthropod born viruses)

*9. Rhabdovirus*9. Rhabdovirus (1) medium size (2) single stranded RNA viruses, helical symmetry (3) bullet shaped envelop (4) intracytoplasmic inclusions (5) transmitted by animal or animal bites (6) eg. vesicular stomatitis, rabies *10. Flavivirus*10. Flavivirus (1) small size (2) enveloped single stranded RNA viruses (3) similar to toga viruses (4) transmitted by mosquitoes or ticks (5) eg. yellow fever, Dengue viruses, St. Louis Encephalitis, Japanese Encephalitis

*11. Togaviruses*11. Togaviruses (1) small size (2) enveloped single stranded RNA viruses (3) complex life cycle involving biting insects (4) eg. Dengue like fever. 

*12. Arenavirus12. Arenavirus (1) medium size (2) enveloped single stranded RNA viruses (3) transmitted by animal or animal bites (4) eg. South American hemorrhagic fever 

*13. Bunyavirus13. Bunyavirus (1) medium size (2) enveloped single stranded RNA viruses (3) all arthropod-borne viruses, transmitted by mosquitoes or ticks (4) eg. California encephalitis

*14. Reovirus14. Reovirus (1) medium size (2) Double stranded segmented RNA viruses (3) transmitted by mosquitoes or ticks (4) in respiratory tract, enteric canal. (5) eg. infantile gastroenteritis  15. Picornavirus15. Picornavirus (1) smallest viruses (2) single stranded RNA viruses (3) enteric and related virus (4) eg. poliomyelitis, common cold.  16. Coronavirus16. Coronavirus (1) medium size (2) single stranded enveloped virus (helical symmetry) (3) eg. Avian infectious bronchitis

17. Retrovirus17. Retrovirus (1) small size (2) enveloped single stranded RNA tumor virus (3) has reverse transcriptase (4) eg. leukemia or sarcoma in mice, AIDS 18. Other viruses18. Other viruses (1) unclassified (2) eg. some slow neurologic disorders.

The measurement of virusesThe measurement of viruses(Assay of viruses )(Assay of viruses ) 1. measured as infectious unit1. measured as infectious unit

a. plaque forming unit (PFU) series dilutions of virus added

to the cells then add soft agar to prevent diffuse away of

viral particles. The infected area can be seen with the

naked eye. This is called “plaques”.

b. Focus forming unit (FFU) : no plaques, cause cell change

morphology and multiply at a faster rate than uninfected

cells. cells are transformed and form foci. Many tumor virus form foci.

2. count the viral particles2. count the viral particles a. direct counta. direct count EM * viral + latex sphere with know concentration. * centrifuge known volume of viral lysate. Then put onto EM grids and counting the virus particles. The calculate the ture no.  b. indirect countb. indirect count (1) turbidity study

OD Once they have been standarized by EM,

then the concentration of virus can be determined use OD.

eg. O.D. 260 = 1. contain 2.1 x 1012 reovirus.

(2) hemagglutination assay(2) hemagglutination assay Many animal viruses, adsorpt to the red blood cells at a specific way. Each virus has many sites, but the max. no. of cells with which any particles can combine

is Two. (dimmer) 

if cell no. > no. of virus dimmer not significant  if no. of virus > cell no. the lattice of cells is formed that settled out in a highly characteristic pattern. i.e. prevent bottom formation (unagglutinated cells) e.g. influenza virus. A good quantitative assay.

The significance of the infectious unit : virus The significance of the infectious unit : virus particlesparticles  For all animal virus, the no. of viral particles is always exceeds the the no. of infectious unit. range 1:10 to 1: 1000 or even less. Reasons:

1. virus preparation contain a majority of noninfectious particles. 2. all the virus are able to cause productive infection, only a small no. are actually successful in doing so. the ratio may represent the probability with which virus particles achieve productive infection.

The Effect of Virus Infection on the Host The Effect of Virus Infection on the Host CellCell 1. Cytopathic Effects2. Inhibition of Host Macromolecular Biosynthesis3. Changes in the Regulation of Gene Expression4. Appearance of New Antigenic Determinants on the Cell Surface. (Change on the Cell Surface)5. Cell Fusion6. Abortive Infection7. persistent Infection Latent8. Modification of Cellular Permissiveness

1. Cytopathic Effects1. Cytopathic Effects With lytic virus, the most easily detected effects of infection with lytic virus.

a. plaque formation is due to the cytopathic effect of virus, plaques are the areas of killed cells. 

b. Using Microscopes or EM can see changes at the cellular level 

i. Nucleus is affected first with pyknosis changes in nucleolar structure, and margination of the chromatin.

ii. Cell Membrane Cell lose ability to adhere round up, sometimes develop a strong tendency to fuse with one another.

iii. Appearance either in the nucleus or in the cytoplasm, distinct spreading foci that are generally composed by fibrillar material (inclusion bodies). It represent the sites of viral detected biosynthesis and morphogenesis. 

iv. Necrotic and degradative changes in the cells become noticeable.

Rapid degradation of the cellular components with the resultant of degradation of the cell.

Characteristic inclusion bodies occur with some viral Characteristic inclusion bodies occur with some viral infections andinfections and

served as useful diagnostic tools.served as useful diagnostic tools. 

Usually within a few days these cell-destroying viruses Usually within a few days these cell-destroying viruses have causedhave caused

enough damage that symptoms of that clinical disease enough damage that symptoms of that clinical disease begin to appear begin to appear

in the host. in the host.

The common acute viral disease are caused by these The common acute viral disease are caused by these cell destroyingcell destroying

virus.virus. 

1. Intranuclear inclusions from a herpes infection (ds linear DNA, enveloped icosahedral) 

2. A rosette -type intranuclear inclusions from an adenoviruse

(ds DNA linear, naked icosahedral) 

3. Intracytoplasmic inclusions from rabies viral infection

(rhabdo virus ss - RNA linear, enveloped, helical) Negri bodies

  

4. Both intranuclear and intracytoplasmic inclusions in the same

cell from a measles viral infection (paramyxovirus enveloped helical -ss linear RNA)

2. Inhibition of Host Macromolecular Biosynthesis2. Inhibition of Host Macromolecular Biosynthesis  The induction of cytopathic effects early after infection may be intimately related to the inhibition of host protein, DNA and RNA synthesis. (in lytic virus - cell interaction).  Host protein synthesis is inhibited first. Inhibition of host protein synthesis then quickly causes inhibition of host DNA replication and then RNA synthesis.  Some exceptions have been reported. * VSV(vesicular stomatitis virus), a Rhabdo virus, G glycoprotein inhibits cell DNA first but not protein synthesis.  * Pox virus, inhibits host DNA synthesis

3. Changes in the Regulation of Gene Expression  Virus infection may also affect the regulation of gene expression.

The activities of enzymes on the pathway of nucleic acid biosynthesis often increases after infection. e.g. papova virus (SV40, polyoma) causes increases in the activities of at least 6 enzymes.

One of these enzymes is deoxypyrimidine kinase that phosphorylates both deoxyuridine and deoxycytidine.

Two forms of this enzyme in cell, one is in the resting cells, the other is in growing cells. When resting cells are infected with SV40 or adenovirus the growing cell type enzymes is induced.

* Infection with almost all virus leads to the synthesis of a new protein Interferon.  

All these suggested that infection upset the regulatory mechanism in normal cells. Usually, during the early parts of the infection cycle, more of the cell genome may be expressed in infected than in uninfected cells.

4. Appearance of New Antigenic Determinants on the 4. Appearance of New Antigenic Determinants on the Cell SurfaceCell Surface 

Outer cell membrane is modified: a. cell morphology changes, they become more agglutinable by lectin concanavalin A. b. permeability increases c. new antigenic determinants appear on the cell surface. 

If it is enveloped virus, the new determinants are likely to be viral envelope proteins. It can also be non enveloped virus. The presence of these determinants serves to alert the immune mechanism.

5. Cell Fusion5. Cell Fusion

Some viruses cause cells to fuse with one another, which results in the formation of giant syncytia, mass of cytoplasm bounded by one membrane that contain hundreds and even thousands of nuclei. This change may be due to the interaction of viral proteins with cell membrane. e.g. paramyxoviruses such as Sendai virus have F spike glycoprotein. herpes glycoprotein gB and gD are involved in this cell fusion. 

This phenomena can cause by active and inactive virus. It can also induce among not only identical but different cells and produce heterokaryons.

HYBRIDOMA 1-5 ARE LYTIC MULTIPLICATION CYCLE  6. Abortive Infection6. Abortive Infection  Some viruses can infect cells but not fully permissive and even cells that are nonpermissive. In the cells, virus can’t multiply because some essential step of the multiplication cycle can’t proceed. e.g. abortive infection of Hela cells by influenza virus monkey cells by human adenovirus. Infection of permissive cells in the presence of antiviral agents is also abortive.  In almost all such cases, the viral genome begins to express itself, the alteration in the host cell appeared (cytopathic effect)

7. Persistent infection7. Persistent infection  Some cases, cell cultures are normal, nevertheless release significant amount of viruses. A balance may be maintained between cell growth and virus multiplication. a. paramyxovirus SV5 infect monkey kidney cells cell divide, viral multiply, cells are infected. This type of infection can’t be cured by the addition of neutralizing antibodies.  b. Lytic but low burst size or low infectivity. The yield is small, viral - cell interaction is lytic. cell die. Many factors reduce the probability of reinfection, the proportion of the infected cells in the total cell population is kept small and constant.

i. This type of infection occurs in almost nonpermissive cells.

ii. factors in the medium, such as antibodies or interferon, prevent the majority of released progeny virus from infecting new virus.

iii. usually the virus are less virulent and less cytopathic.

  defective interfering particles (DI) virus yields from persistently infected cells

sometimes contain a deletion mutants, it can’t multiply on their own, is able to interfering with the multiplication of the infectious virus.

i.e. there presence reduces both cell damage and the amount of infectious virus that is produced.

  This kind of persistent infection can be cured by

the addition of large amount of neutrolizing antibody.

8. Latency8. Latency 

Persistent infection with no viral progeny.

The viral multiplication can start but arrested at some stage or other. e.g. herpesviruse. If the condition is right, it will release infectious virus.  e.g. latent herpes simplex type I, neurons of sensory ganglia fever blisters due to: latent herpes DNA is heavily hypermethylated, hypermethylation is known to reduce gene expression very significantly.  Other persistent infection of latent type tend to cause progressive disease. e.g. sub-acute sclerosing panencephalitis (SSPE), an infection of the central nervous system by a virus closely related to measles.

Large amount of viral nucleocapsids are present in infected cells. 

A progressive multifocal leukoencephalopahty (PML) by papova virus infection.

9. Modification of Cellular Permissiveness9. Modification of Cellular Permissiveness

Occasionally, virus infection can alter the cellular permissiveness for completely unrelated viruses. (usually very specific) 

e.g. adeno-associated virus can only infect the cell with adenovirus. 

SV40 enable human adenoviurus to grow in monkey cells. 

pox virus, such as vaccinia, enable VSV to multiply in rabbit cells. 

The helper functions appear always to involve translation of mRNA, i.e. protein synthesis.

e.g. VSV alone in rabbit cornea cells no VSV proteins are synthesized, VSV protein synthesis is inhibited at the stage of elongation.

vaccinia virus

  VSV multiplies normally i.e. vaccinia virus modify the protein synthesis mechanism of VSV, therefore, protein synthesis normally.