PG AND RESEARCH DEPARTMENT OF MICROBIOLOGY - SRI PARAMAKALYANI COLLEGE - ALWARKURICHI

1. SRI PARAMAKALYANI COLLEGE
( Reaccredited with B Grade with a CGPA of 2.71 in the II Cycle by NAAC
Affiliated to Manonmaniam Sundaranar University, Tirunelveli)
ALWARKURICHI 627 412 TAMIL NADU, INDIA
POST GRADUATE & RESEARCH CENTRE - DEPARTMENT OF MICROBIOLOGY
(Government Aided)
II SEM - CORE –VIROLOGY
SUB CODE: ZMBM23
UNIT I
NUCLEIC ACID STRUCTURE AND EVOLUTION OF VIRUS
SUBMITTED TO C. SARANYA VELLAIAMMAL
GUIDE: Dr. C. MARIAPPAN, Ph.D REG NO : 20211232516124
ASSISTANT PROFESSOR I. M.SC.MICROBIOLOGY
SRI PARAMAKALYANI COLLEGE SRI PARAMAKALYANI COLLEGE
ALWARKURICHI ALWARKURICHI

2. CONTENTS
 Nucleic acid structure
 Viral genome classification
 Baltimore classification
 Genome size
 Evolution of virus
 The potential for rapid evolution in viruses
 Evolution of measles virus
 Evolution of myxoma virus
 Evolution of influenza virus

3. NUCLEIC ACID STRUCTURE OF
VIRUS
 It is a microscopic, simple infectious agent that can multiply only in living
cells of animals, plants, or bacteria.
 Viruses are much smaller than bacteria
 It consists of a single- or double-stranded nucleic acid (DNA or RNA)
surrounded by a protein shell called a capsid.
 Some viruses also have an outer envelope composed of lipids and proteins.
They vary in shape.

4.  The genes of viruses are made from DNA (deoxyribonucleic acid) and, in
many viruses, RNA (ribonucleic acid).
 The biological information contained in an organism is encoded in its DNA
or RNA.
 Most organisms use DNA, but many viruses have RNA as their genetic
material.
 The DNA or RNA of viruses consists of either a single strand or a double
helix.
 Any particular virus contains only a single kind of nucleic acid.

5.  Molecules on virus surface impart high specificity for attachment to host
cell.
 Multiply by taking control of host cell’s genetic material and regulating the
synthesis and assembly of new viruses.
 Lack enzymes for most metabolic processes.
 Lack machinery for synthesizing proteins.
 Most RNA viruses multiply in & are released from the cytoplasm.
 Viral infections range from very mild to life threatening.

6.  viruses that infect plants have single-stranded RNA
 viruses that infect animals have either single or double-stranded RNA or
double-stranded DNA
 bacteriophages (viruses that infect bacteria) are usually double-stranded
DNA viruses.

7. VIRAL GENOME
CLASSIFICATION

8. BALTIMORE CLASSIFICATION
 Baltimore classification is a system used to classify viruses based on their
manner of messenger RNA (mRNA) synthesis. By organizing viruses based on
their manner of mRNA production, it is possible to study viruses that behave
similarly as a distinct group.
 Baltimore classification was created in 1971 by virologist David Baltimore
 There are seven Baltimore groups numbered with Roman numerals
 Baltimore classification is chiefly based on the transcription of the viral
genome

11. VIRAL GENOME SIZE
 Virus genomes span a large range of sizes.
 Porcine circovirus (ssDNA) and hepatitis delta virus (ssRNA) each have
a genome of about 1.7 kilobases (kb), while at the other end of the scale
there are viruses with dsDNA genomes comprised of over 1000 kilobase
pairs (kbp).
 The largest RNA genomes known are those of some coronaviruses, which
are 33 kb of ssRNA.

12. EVOLUTION OF VIRUS
 Viral evolution is a subfield of evolutionary biology and virology that is
specifically concerned with the evolution of viruses.
 Viruses have short generation times, and many—in particular RNA
viruses—have relatively high mutation rates
 Viruses typically produce many copies in an infected host, mutated genes
can be passed on to many offspring quickly.
 Although the chance of mutations and evolution can change depending on
the type of virus, viruses overall have high chances for mutations.

13.  The two prevailing opinions are that viruses have either arisen
(i) from degenerate cells that have lost the ability for independent life, and
(ii) from escaped fragments of cellular nucleic acid.
 Viruses are largely species-specific with respect to their host and usually do
not cross species boundaries.

14. VIRUS EVOLUTION

15. THE POTENTIAL FOR RAPID
EVOLUTION IN RNA VIRUSES
 Quasispecies
 Rapid evolution

16. QUASISPECIES
 The lack of a proofreading function in the polymerases of RNA viruses
means that base substitutions (mutations) occur at the rate of between 10−3
and 10−5 per base per genome replication event.
 Not all of the resulting mutants will be viable but many are, resulting in an
extremely heterogeneous population of viruses. This is called a
quasispecies.
 For example, it is not possible to define the genome sequence of that virus
population precisely, and any sequence in a database will represent only one
member of the quasispecies.

17. QUASISPECIES CLOUD

18.  The micro level is infection of the individual, and virus evolution during the
life time of the individual is seen, particularly in life-long infections with
HIV-1 (see Chapter 19) and hepatitis C virus.
 The macro level of evolution is seen in viruses with a worldwide
distribution.
 The virus evolves with the effect that approximately 4 years, it is not
recognized by the immune memory established by the original host, and
he/she can be reinfected. This is called antigenic drift, and essentially
results in the formation of new serotypes of virus.

19. RAPID EVOLUTION
RECOMBINATION
 Recombination is the other major force in virus evolution and takes place in
a cell that is simultaneously infected by two viruses.
 Usually, the two genomes are highly related with regions of homology
between their genomes that permit the replicating enzyme to move from one
strand to another.
 Both parts of the resulting genome have to be sufficiently compatible for
the progeny to be functional.

20.  Viruses with segmented genomes can also undergo recombination by
acquiring an entire genome segment from another virus, and this occurs at
higher frequency. This form of recombination is known as reassortment.
 The effect on antigenicity is enormous as a virus can acquire an entirely
new coat protein in a single step. The prime example is influenza A virus
where this process, called antigenic shift, is responsible for pandemic
influenza in man.

22. EVOLUTION OF MEASLES VIRUS
 F. L. Black studied the occurrence of the measles in island populations and
found a good correlation between the size of the population and the number
of cases of measles recorded on the island throughout the year.
 A population of at least 500,000 is required to provide sufficient susceptible
individuals (i.e. new births) to maintain the virus in the population.
 Below that level, the virus eventually dies out, until it is reintroduced from
an outside source.

23.  Black has speculated upon the antigenic similarity of measles, canine
distemper, and rinderpest viruses.
 Black suggests that these three viruses have a common ancestor which
infected prehistoric dogs or cattle.
 The ancestral virus evolved to the modern measles virus when changes in
the social behavior of humans gave rise to populations large enough to
maintain the infection.
 The first such population occurred 6000 years ago when the river valley
civilizations of the Tigris and Euphrates were established.

24. EVOLUTION OF MYXOMA VIRUS
 In Australia, myxoma virus infected rabbits were released in the wild but,
despite the virulence of the virus and the presence of susceptible hosts, the
virus died out.
 It was then realized that this was due to the scarcity of mosquito vectors.
 The investigators then compared the virulence of the original virus with
virus newly isolated from wild rabbits by inoculating standard laboratory
rabbits.

25.  Two significant facts emerged:
(i) rabbits infected with new virus isolates took longer to die, and
(ii) a greater number of rabbits recovered from infection. From this it was
inferred that the virus had evolved to a less virulent form.
 The second finding concerned the rabbits themselves, and the possibility
that rabbits were evolving resistance to myxomatosis.

26. MYXOMATOSIS SYMPTOMS

27. EVOLUTION OF INFLUENZA VIRUS
 There are three groups of influenza virus, types A, B, and C.
 Type A viruses cause the worldwide epidemics (pandemics) of influenza,
and both type A and B viruses cause epidemics.
 The primary hosts of influenza A viruses are wild aquatic birds (such as
ducks, terns, and shore birds). Influenza B viruses infect only humans.

28. FLU VIRAL EVOLUTION

29. REPLICATION

30. TWO MECHANISMS OF EVOLUTION
 Influenza A viruses undergo two types of change affecting their major
surface glycoproteins called antigenic shift and antigenic drift.
 A shift results in a pandemic, is always preceded by an abrupt change in
hemagglutinin subtype and, apart from the 1968 virus, also by a change in
neuraminidase subtype.
 Drift results in epidemics, and is caused by gradual evolution under the
positive selection pressure of neutralizing antibody.

31.  A new shift virus immediately starts to undergo continuous antigenic drift.
 Influenza B viruses only undergo drift and this is believed to be because
they infect only man and have no other animal reservoir.
 These viruses are highly infectious and cause an acutely cytopathogenic
infection.
 They have evolved strategies for changing their antigens in order to
increase the proportion of susceptible individuals in the population.

33. ANTIGENIC DRIFT AND SHIFT

34. REFERENCE
 Introduction to Modern Virology Paperback – 14
December 2006 by Nigel Dimmock (Author), Andrew
Easton (Author), Keith Leppard (Author)