this ppt is about general introduction of virus.

1. Virus
Ranjeet Kumar Taram
SoS in Life Science
Pt. Ravishankar Shukla university Raipur

2. • Virus
• Virus is defined as a nucleoprotein complex a small infectious agent which infect cell and uses
their metabolic machinery to replicate. It is simple acellular entities.
• Characteristics :-
• Obligate intracellular parasites of bacteria, protozoa, algae, fungi, plants and animals.
• Ultramicroscopic size ranging from 20 nm to 400 nm diameter.
• All viruses have a nucleocapsid composed of a nucleic acid genome surrounded by a protein
capsid. Some viruses have a membranous envelope that lies outside the nucleocapsid.
• The nucleic acid of the virus can be RNA or DNA, single-stranded or double stranded, linear or
circular.
• Capsids may have helical, icosahedral, or complex symmetry. They are constructed of protomers
that self-assemble through noncovalent bonds.
• The typical virus life cycle consists of five steps: attachment to the host cell, entry into the host
cell, synthesis of viral nucleic acid and proteins within the host cell, self-assembly of virions
within the host cell, and release of virions from the host cell
• Viruses are not affected by antibiotics ,affected only by antiviral drugs and interferons.

3. Historical account
• The Russian botanist Ivanovski (1892) was the first to give clear cut evidence of a virus
• M.Beijerinck (1897)was first to coined the term virus.
• Bacteriophages were discovered by Twort and D. Herelle(1917).
• Schelsinger (1933)was the first to determine the composition of a virus. He showed that a
bacteriophage consists of only protein and DNA.
• In 1935, Stanley crystallized the virus causing tobacco mosaic disease and demonstrated that
crystals retained their infectivity when inoculated into healthy plants.
• In 1952, Hershey and Chase studied the T2 bacteriophage and demonstrated that the genetic
information is carried in the phage DNA and that infection is the result of penetration of viral DNA
into cells.

4. Classification
• Virus classification is the process of naming viruses and placing them into taxonomic system.
• Before discovery:-
i. Dermotrophic – infect skin cells.
ii. Neurotrophic - infect nerve cells.
iii. Viscerotrophic - infect digestive tract.
iv. Pneumotrophic - infect respiratory system.
After discovery viruses are classified on the basis of –
Types and structure of their nucleic acid.
Method of replication.
Host range.
Chemical and physical characteristics.

5. • ICTV(International committee on Taxonomy of viruses) is responsible for the classification of
the viruses.
• Suffixes used for classification –
•
Taxa Suffix For ex. –Rhabdovirus
Realm Viria Riboviria
Kingdom Virae Orthonavirae
Phylum Viricota Negarnaviricota
Class Viricetes Monjiviricetes
Order Virales Mononegavirales
Family Viridae Rhabdoviridae
Genus Virus Rhabdovirus

6. • On the basis of morphology virus capsids are classify as –
1. Icosahedral capsid – in this type of capsid 20 triangular faces and 12 corner or vertices are
present with regularly arranged unit called capsomers and nucleic acid is densely coiled.
a) Naked capsid – Adeno virus, Polio virus.
b) Enveloped capsid - Herpes Simplex virus.
2. Helical capsid – in this type of capsid shaped like hollow tube with protein walls.
Protomers are arranged helical or spirals and produce long rigid tube like structure and capsid
enclosed nuclear material.
a) Naked capsid – TMV, bacteriophage tail.
b) Enveloped capsid – Influenza virus.
3. Complex capsid – most viruses have either icosahedral or helical symmetry but some viruses are
not classified as above they placed in the complex capsid category.
Ex.- Bacteriophage, Vaccinia virus, Pox virus etc.

7. Fig.-Icosahedral Capsid
Fig.-Helical Capsid
Fig.-Complex Capsid

8. Baltimore classification
• David Baltimore and Howard Temin gave the Baltimore classification system.
• This classification is based on genome type and mode of replication and transcription.
Class Description of genome and replication strategy Example
I Double stranded DNA (ds DNA) Herpes virus, Pox virus
II Single stranded DNA (ss DNA) Pervovirus
III Double stranded RNA (ds RNA) Reovirus
IV Single stranded RNA with positively sensed (+ss RNA) Picornavirus, Flavivirus
V Single stranded RNA with negatively sensed (-ss RNA) Influenza virus,
Rhabdovirus
VI Single stranded RNA genome that replicated with DNA intermediate (ss RNA- RT) Retrovirus
VII Double stranded DNA genome that replicates with RNA intermediate (ds DNA) Hepadnavirus, Hepatitis B
virus

9. Tobacco Mosaic virus (TMV)
• Introduction
• TMV is the most serious plant pathogen causing
mosaic on tobacco plant.
• It is a plant virus that have positive single
stranded RNA that infects a wide range of plant
especially tobacco and Solanaceae family.
• TMV is the most resistant virus known so far of
which the thermal death point is 90˚C for 10
min.
• This is the first virus that was crystallized in
1935 by W. M. Stanley.
Kingdom Orthonavirae
Phylum Kitrinoviricota
Class Alsuviricetes
Order Martellivirales
Family Virgaviridae
Genus Tobamovirus
Species Tobacco mosaic virus
Classification

10. • Structure :-
• It is a rod shaped helical virus about 300 nm long
and 15-18 nm in diameter.
• It consist of capsid made from 2130 capsomeres
arranged in a hollow right handed helix.
• It contains a single stranded RNA of 6400
nucleotide.
• Each protein subunit is made up of a single
polypeptide chain consisting of 158 amino acid
residue whose sequence has been established.
• This protein self assemble to form a hairpin loop
structure.
• The molecular weight of TMV is 2.06x106 Dalton.

11. • Mode of infection:-
• TMV enters plants through wounds, Damage
to the plant cell membrane and permit entry
of infectious particle into cytoplasm.
• The virus spreads from an initial infection
site to all parts of the plant via the phloem,
the plants nutrient transport network.
• It is also transported by mechanical means in
the field by wind or water.
Fig.- Pathogenicity of TMV

12. • Symptoms
• Symptoms include mosaic pattern on
leaves, mottling, necrosis and leaf
curling.
• The lighting of leaf color among the
veins in early stage.
• In later stage, it turn into light and
dark green mosaic symptoms.
• Yellow streaking of
leaves.(especially monocots)
• Yellow spotting on leaves.

13. • Control
• TMV occurs in tobacco growing areas so it is controlled by crop rotation.
• Crop rotation should also be employed to avoid infected soil/ seed beds for at least two
years.
• One of the common control methods for TMV is sanitation, which includes removing
infected plants and washing hands in between each planting.
• As for any plant disease, looking for resistant strains against TMV may also be advised.
• The proliferation of aphids will aid in the spread of foliar diseases, and killing them can
effectively reduce the rate of foliar disease infection. Aphid control can be carried out with
the choice of oxaliplatin, vanillin, imidacloprid, etc.
• Spraying with disinfectant can be used for prevention during agricultural processes such
as leaf-cutting, seed removal, and topping, and can last for two weeks at a time.

14. Cucumber Mosaic Virus (CMV)
• Introduction
Cucumber mosaic virus (CMV) is one of the most
widespread and troublesome viruses infecting
cultivated plants worldwide.
The virus is made up of many and varied strains
that differ in a number of aspects including host
range, symptoms, and means of transmission.
The strains of CMV are differentiated on the basis
of symptoms on indicator host plants.
Classification
Realm Riboviria
Kingdom Orthornavirae
Phylum Kitrinoviricota
Class Alsuviricetes
Order Martellivirales
Family Bromoviridae
Genus Cucumovirus

15. • Structure
• Virion- non-enveloped, spherical virion about
29 nm in diameter with T=3 icosahedral
symmetry, composed of 180 coat proteins,
12pentamers and 20 hexamers.
• The capsid is composed of 60 asymmetric
units made of 3 protein (T=3) ,for a total 180
capsid proteins.

16. • Genome- segmented, tripartite linear
positively sensed ss RNA(+).
• Its genome size is 8.623 kb and it is divided
among RNA1(3357bp), RNA2(3050 bp) and
RNA3(2216 bp), all of which has a tRNA-like
structure and 5’ cap.
• These three RNAs encode five proteins,
proteins 1a, 2a, 2b, movement protein (MP)
and coat protein (CP).
• proteins 1a and 2a are responsible for the
replication of the virus, protein 2b is the host-
silencing suppressor(viral suppressor of RNA
silencing VSR).

17. Mode of infection
• Virus transmission-
• Arthropods: - CMV is vectored and
transmitted by cucumber beetles and more
than 60 species of aphids.
• Mechanically: - CMV is readily
transmitted between plants via plant sap
and by mechanical inoculation via pruning
tools.
• Seeds: - Transmission to new plants
through seeds occurs to varying degrees
for 19 host species, including some
important weeds.
• Parasitic seed plants:- This virus can also
be transmitted between plants by parasitic
seed plants such as dodder (Cuscuta spp.),
whose vine-like stems bridge the hosts
aerially or at the ground surface.

18. Life cycle of virus in host plant.
1.Virus penetrates into the host cell.
2.Uncoating, and release of the viral genomic RNA into the cytoplasm.
3.Expression of protein 1a and 2a to produce replication proteins.
4.Replication occurs in viral factories made of membrane vesicles derived from the
ER (spherules). A dsRNA genome is synthesized from the genomic ss RNA(+).
5.The dsRNA genome is transcribed/replicated thereby providing viral mRNA/new
ssRNA(+) genomes.
6.Subgenomic RNA4 is translated producing capsid proteins.
7.Assembly of new virus particles.
8.Viral movement protein triggers the formation of tubular structures that mediate
virion cell-to-cell transfer via a tubule-guided mechanism.

19. • Symptoms
Cucurbit plants may become infected at stage of growth, from
emergence of the seedling to near maturity.
CMV symptoms in cucumber are more severe on plants exposed to
short days or reduced light than on plants exposed to long days and
bright light.
Cucurbit plants rarely become infected in the seedling stage. When
this happens, the cotyledons may turn yellow and wilt.
New leaves are slightly mottled a yellowish green, remain small,
wrinkled, and distorted. Plants infected in the seedling stage remain
dwarfed or may die.
Leaves are often stunted, distorted, crinkled, and curled downward.
Vines are sometimes dwarfed and may be yellowish near the center
of the hill and "bunchy" because of shortening of the stem between

21. • Disease management
• Manage infected weeds and alternate hosts for CMV and vectors before planting.
• Exclude CMV from production houses. Exclusion in a production house means physically
preventing CMV from infecting susceptible hosts.
• Manage aphids and CMV in production houses before out planting. Establish host-free zones
around production houses by using cement, mulch, rocks, or herbicides to reduce nearby vector
and virus populations. Apply insecticides within production houses to minimize vector numbers.
• Plant CMV-resistant host varieties. Resistant plants are the best management practice, because
they require fewer inputs, are easy to use, and don’t have adverse effects on the environment.
• Fumigate greenhouses regularly to control aphids and other insects.
• Apply insecticides regularly in and around the greenhouse, garden, or field to eliminate aphids,
cucumber beetles, and other insects. It is important to kill insects before they have an opportunity
to infect vine crops and move from plant to plant in a cucurbit planting.

22. Human Immunodeficiency Virus (HIV)
• The human immunodeficiency virus is a lentivirus that
causes the acquired immunodeficiency syndrome (AIDS),
a condition in humans in which progressive failure of the
immune system allows opportunistic infections and
cancers to prosper.
• Unlike some other viruses, the human body cannot get rid
of HIV. That means that once you have HIV, you have it
for life.
• Scientists identified a type of chimpanzee in West Africa
as the source of HIV infection in humans. They believe
that the chimpanzee version of the immunodeficiency
virus (called simian immunodeficiency virus, or SIV)
most likely was transmitted to humans and mutated into
HIV when humans hunted these chimpanzees for meat
and came into contact with their infected blood. HIV was
first described in USA in 1981 amongst homosexuals,
Haitians and heroine addicts.
Realm Ribovira
Kingdom Pararnavirae
Phylum Artverviricota
Class Revtraviricetes
Order Orthovirales
Family Retroviridae
Subfamily Orthoretrovirinae
Genus Lentivirus
Species HIV1 /HIV2

23. Morphology
• It is roughly spherical - diameter of about 120 nm.
• Composed of two copies of positive single stranded RNA (Held together by
protein P7) enclosed by a conical capsid composed of viral protein P24
• Very high genetic variability.
• The RNA genome consists of 9 genes - Three of these genes: gag, pol, and
env, contain information needed to make the structural proteins for new
virus particles.
• Inside of capsid are three enzymes required for HIV replication: reverse
transcriptase, integrase and protease.
• A matrix composed of the viral protein P17 surrounds the capsid ensuring
the integrity of the virion particle.
• The matrix is surrounded by phospholipids – 2 layers – Embedded by 70
copies of a complex HIV protein (glycoprotein) – Spikes: 2 units – Gp41
and Gp120.

25. Mode of transmission

27. • Attachment-Attachment of virus into the host cell by Specific binding of the virus to the CD4
receptors is by the envelope glycoprotein gp120.
• Cell to cell fusion – For infection to take place the cell fusion is essential.
• This is brought about by the transmembrane glycoprotein gp 41. HIV-1 utilizes two major co-
receptors along with CD4 to bind to, fuse with, and enter target cells; these co-receptors are
CCR5 and CXCR4, which are also receptors for certain endogenous chemokines.
• Strains of HIV that utilize CCR5 as a co-receptor are referred to as macrophage tropic viruses
(M –tropic viruses)
• Strains of HIV that utilize CXCR4 are referred to as T - tropic viruses.
• Many virus strains are dual tropic in that they utilize both CCR5 and CXCR4.
• Uncoating of the viral envelope and entry of nuclear capsid core into the cell , After fusion of
virus with the host cell membrane, HIV genome is uncoated and internalized in to cell. Viral
RNA is released into the core cytoplasm
Life cycle of HIV

28. • Viral transcription
• Viral reverse transcriptase mediates transcription of its RNA.
• RNA-DNA hybrid is formed .
• Original RNA strand is degraded by ribonuclease H, followed by.
• Synthesis of second strand of DNA to yield double strand HIV DNA.
• Integration into the host DNA
• The double stranded DNA bis integrated in to the genome of the infected host cell through the action of
the viral integrase enzyme , causing a latent infection.
• Fate of provirus
• From time to time, lytic infection is initiated releasing progeny virions, which infect other cells.
• The long and variable incubation period of HIV is because of the latency.
• In an infected individual the virus can be isolated from the blood , lymphocytes, cell free plasma, semen ,
cervical secretion, saliva, urine and breast milk.

29. • Transcription back into RNA
• The viral DNA is transcribed into RNA and multiple copies of viral RNA are produced.
• There are only nine gene in HIV RNA, and these code for the production of structural proteins,
accessory proteins and enzymes that essential for the virus's replicative cycle.
• Virion assembly- With the help of viral protease the new virion are assembled into the
polypeptide sequences needed for HIV virion formation and infectivity.
• Cell lysis- the infected cell is made to burst open, presumably by the action of cellular proteins.

31. Treatment
• There are two principal approaches to treatment :- immunotherapy and anti-HIV drug treatments.
• A. Immunotherapy:-
Immunotherapy is transfusion based treatment designed to replace lost immunoglobulins needed to fi
ght HIV infection (passive immunotherapy), to provide cellular factors such as interleukins
(IL2) or to introduce selected or altered immune cells to attack cells harboring the virus (adoptive im
munotherapy).
• B. Anti-HIV drug treatment:-
• Treatment with anti-HIV drugs attempts to reduce viral load by blocking new infection in the host
cell.
• The drugs target two major enzymes of HIV which are needed for the infection cycle: Reverse
transcriptase and Proteases.
• Ex.- Nucleoside Reverse transcriptase inhibitor- zydovudine, stavudine.
• Non-nucleoside Reverse Transcriptase inhibitor – Efavirenz, Nevirapine.
• Protease inhibitor – Atazanavir, Darunavir.

32. Treatment
C. Combination Treatment :-
Since reverse transcriptase inhibitors and protease inhibitor address different stage of viral
replication, using both families of drugs in combination has been shown to be more
effective than monotherapy in impending the spread of HIV in the body and reducing viral
loads.
This communication of two reverse transcriptase inhibitor, one of which is a thymidine
analogue, and a protease inhibitor, block infection both before and after integration and in
both activated and resting T cells.
This combinational therapy is termed as highly active anti-retroviral therapy.
D. In future :-
In addition to the positive results shown by combination therapy trials, a number of
development may hold promise for the near future.
These include genetically engineered killer T cells which attack HIV before it reproduces,
and research into genetically deactivating the CXCR4 and CCR5 T cell co-receptors, which
are a path for HIV entry into cells.

33. Prevention
• There is no vaccine to prevent HIV infection and no cure for AIDS. But it is
possible to protect ourself and other from infection.
• It means educating everyone about HIV and avoid any behavior that allows
HIV infected fluids into our body.

34. Herpes virus
• Herpes is the name of a group of viruses that causes painful
blister and sore.
• These viruses are enveloped and show host specificity.
• They are double stranded DNA viruses with relatively large
complex genomes and replicate in the nucleus of a wide
range of vertebrate hosts.
• Herpes simplex is a viral infection that typically affects the
mouth, genital or anal area .
• It is contagious and can cause outbreak of sores and other
symptoms.
• These are blister that develop on the surface of the skin and
may be itchy or uncomfortable.
• Herpes virus have ability to persist indefinitely in their host
by establishing latent infection that may lead to recurrent
symptoms.
Classification
Realm Duplodnaviria
Kingdom Heunggongviriae
Phylum Peploviricota
Class Hervivicetes
Order Herpesvirales
Family Herpesviridae
Genus Simplex virus

36. Morphology
• All herpesvirus virions have four structural elements:-
• Core. The core consists of a single linear molecule of dsDNA in the form of a torus.
• Capsid. Surrounding the core is an icosahedral capsid with a 100 nm diameter constructed of 162
capsomeres.
• Tegument. Between the capsid and envelope is an amorphous, sometimes asymmetrical, feature
named the tegument. It consists of viral enzymes, some of which are needed to take control of the
cell's chemical processes and subvert them to virion production, some of which defend against the
host cell's immediate responses, and others for which the function is not yet understood.
• Envelope. The envelope is the outer layer of the virion and is composed of altered host
membrane and a dozen unique viral glycoproteins. They appear in electron micrographs as short
spikes embedded in the envelope.

37. Morphology
Genome structure
The herpes virus genome contain a non-
segmented, linear , ds- DNA molecule.
Genome length range approximately 120 to 250
kbp and encode for 60-120 genes.
HSV-1 and HSV-2 each contain at least 74 genes
within their genome.
These genes encode a variety of proteins
involved in forming the capsid, tegument and
envelope of the virus, as well as controlling the
replication and infectivity of the virus.

38. Life cycle of Herpes virus

39. Pathogenicity
Stages Of Infections:- their are different stages of infection:-
(i) Primary Stage :-
This stage starts 2 to 8 days after infection.
The area under the blister will be red and painful, the fluid in the blister may be cloudy.
The blister break and become open sores.
(ii) Latent Stage:- during this stage, there are no blister, sores or other symptoms. The virus is
travelling from skin into the nerves .
(iii) Shedding Stage:- in the shedding stage, the virus starts multiplying in the nerve ending.
If these nerve ending areas of the body that are in contact with body fluids, include- saliva, semen
or vaginal fluid , this means that herpes is very contagious during this stage.

40. • Treatment
• Infections with herpes simplex virus 1
and 2 and varicella-zoster virus are
currently the most amenable to
therapy; acyclovir, valaciclovir and
famciclovir are all licensed
therapeutics.
• Alternatively, zinc containing cream or
slightly anesthetic cream can be
applied.
• Prevention
• People with active symptoms of oral
herpes should avoid oral contact with
other.
• A vaccine to prevent varicella-zoster
virus infections was recently licensed
in the United States. Vaccines against
herpes simplex virus 2, and
cytomegalovirus are undergoing
extensive evaluations in field trials.
• Passive immunization with
immunoglobulin or hyperimmune
globulin is used either to prevent
infection or as an adjunct to antiviral
therapy.

41. Pox virus
• Introduction
• Term “pox” derives from English pocks,
blister like skin lesions.
• Pox virus infection typically result in the
formation of lesions, skin nodules or
disseminated rashes.
• Family pox virideae causes various disease,
small pox is one of them.
• Small pox is an infectious, contagious and
some times fatal disease unique only in
human.
• It is caused by either of two Variola virus:-
• 1.Variola major
• 2. Variola minor.
Classification
Realm Varidnaviria
Kingdom Bamfordvirae
Phylum Nucleocytoviricota
Class Pokkesviricetes
Order Chitovirales
Family Poxviridae
Genus Orthopoxvirus
Species Variola virus

42. Morphology
• Pox virus are largest virus, size
300x200x100 nm with a single
linear double stranded DNA genome
186 kbp in size and containing a hairpin
loop at each end.
• It consist of central biconcave DNA
core.
• Brick or oval shape.

43. Life cycle of Pox virus
Abbreviation:-
EEV- External Enveloped Virion
IEV- Intracellular Enveloped Virion
IMV- Intracellular Mature Virion
CEV- Cell-associated Enveloped Virion

44. Even though they are DNA viruses, poxviruses replicate in the cytoplasm. Accordingly, they are
only minimally dependent on the host cell for DNA and RNA replication, and they encode their
own proteins for these processes.
• Step 1- attachment and entry of EEV- The mechanisms by which either the IMV or the EEV
infectious forms of vaccinia virus attach to and enter susceptible host cells are not well
understood and will be constrained by the number of membranes enveloping the virus. After
fusion of the viral and cellular membranes, primary uncoating takes place, and the viral core is
released into the cytoplasm.
• Step 2- All later steps in the infectious cycle take place in this cellular compartment. The core
contains, in addition to the viral genome, the viral DNA-dependent RNA polymerase, the
‘‘initiation’’ proteins necessary for specific recognition of the promoters of viral early genes, and
several RNA processing enzymes that modify viral transcripts.
Life cycle of Pox virus

45. • Step 3- On release into the host-cell cytoplasm, the core synthesizes viral early mRNAs, which
exhibit the features typical of cellular mRNAs and are translated by the cellular protein-
synthesizing machinery. Approximately half of the viral genes are expressed during this early
phase of infection.
• Step 4- Some early proteins are secreted from the cell and have sequence similarity to cellular
growth factors, which can induce proliferation of neighboring host cells, or are proteins that
counteract host immune defense mechanisms.
• Step 5 - The synthesis of early proteins also induces a second uncoating reaction in which the
core wall opens and a nucleoprotein complex containing the genome is released from the core.
• Step 6- This core disassembly leads to cessation of viral early gene expression. Other early
proteins catalyze the replication of the viral DNA genome.

47. • Step 7and 8 - Newly synthesized viral DNA molecules can serve as templates for additional
cycles of genome replication , and they are the templates for transcription of viral intermediate-
phase genes.
• Step 9 -The activation of transcription of intermediate genes also requires specific viral proteins
(the products of early genes) that confer specificity for intermediate promoters on the viral RNA
polymerase, as well as a host-cell protein (Vitf2) that relocates from the infected cell nucleus to
the cytoplasm.
• Step 10- The proteins encoded by intermediate mRNAs include those necessary for
transcription of late-phase genes. The latter genes encode the proteins from which virions are
built as well as the virion enzymes and other essential proteins, such as the early initiation
proteins, that must be incorporated into virus particles during assembly.

48. • Step 11 – once these protein are synthesized by the
cellular translation machinery the assembly of
progeny virus particles begins.
• Step 12- The viral membrane proteins are un-
glycosylated, and the role of cellular membranes in
early stages of assembly is controversial.
• Step 13- The initial assembly reactions result in
formation of the immature virion , which is a
spherical particle delimited by a membrane that
may be acquired from an early compartment of the
cellular secretory pathway.
• Step 14&15- This virus particle matures into the
brick shaped IMV, which is released only on cell
lysis.

49. • Step 16- However, the particle can acquire a
second, double membrane from a trans Golgi
or early endosomal compartment to form the
intracellular enveloped virion (IEV) .
• Step 17- The IEVs move to the cell surface
on microtubules where fusion with the plasma
membrane forms cell-associated virions
(CEV).
• Step 18- These CEV induce an actin
polymerization that promotes a direct transfer
to surrounding cells; they can also dissociate
from the membrane as EEV.

51. Pathogenicity:-
This is airborne disease therefore it spread readily.
Incubation period 7-17 days.
Initial symptoms (Prodrome)
duration – 2 to 4 days which is sometimes contagious
Early rash – (duration: about 4 days) most contagious
Rash distribution
Pustular rash – (duration: about 5 days) –contagious
pustules and scabs –(duration: about 5 days)- contagious
resolving scabs – (duration : about 6 days)- contagious
Scabs resolved – not contagious
smallpox may be most contagious during prodrome phase.
Most infectious during the first 7 to 10 days following rash
onset .

52. Mode of infection:-
Prolonged face-to-face contact
with someone who has smallpox .
Direct contact with infected
bodily fluids or an object such as
bedding or clothing that has the
virus on it.
Exposure to an aerosol release of
smallpox (the virus is put in the
air ).
Treatment
There is no proven
treatment for small pox.
Prevention
• The smallpox vaccine is made from a
virus called vaccinia which is a pox
type virus related to smallpox .
• The smallpox vaccine contain “live”
vaccinia virus – not dead virus like
many other vaccines.
• Edward Jenner (1796)- first successful
vaccine to be developed against
smallpox using cowpox
virus(variolation) .
• The only smallpox vaccine currently
licensed by the food and drug
administration is Dryvax .

53. • One of the most serious bioterrorist threats.
• It is used as a biological weapon during the French and the Indian wars(1774 to1776)when
British soldiers distributed smallpox infected blankets to American Indians .
• several factors contribute to the concern about the use of smallpox as a biological weapon
1) Variola can spread easily from person to person.
2) There is no widely available or licensed treatment for the disease .
3) High fatality rate.
4) Variola is relatively stable as an aerosol.
5) Infectious dose is small.
Small pox as biological weapon