Microbiology - Noncellular Microbes - Louis Carlo Lim

Microbiology and Parasitology
Liceo de Cagayan University, College of Arts and
Sciences
Natural Sciences Department, B.S. Biology

• Differentiate a virus from a bacterium
• Describe the chemical and physical structure of both an enveloped and a
nonenveloped virus.
• Define viral species and give an example of a family, genus, and
common name for a virus.
• Describe how bacteriophages are cultured.
• Describe how animal viruses are cultured.
• List three techniques used to identify viruses.
• Compare and contrast the multiplication cycle of DNA- and RNA-
containing animal viruses.
• Define oncogene and transformed cell.
• Discuss the relationship between DNA- and RNA- containing viruses and
cancer.
• Provide an example of a latent viral infection.
• Discuss how protein can be infectious.
• Differentiate virus, viroid, and prion.

 The question of whether viruses are living
organism has an ambiguous answer.
 Viruses are inert outside living host cells &
generally not considered living organisms.
 Once viruses enter a host cell, the viral
nucleic acids become active and viral
multiplication results & become alive.
 Obligatory intracellular parasites

Viruses Entitle that:
 Contain a single type of nucleic acid, either
DNA or RNA.
 Contain a protein coat (sometimes itself
enclosed by an envelope of lipids, proteins,
and carbohydrates) that surrounds the
nucleic acid.
 Multiply inside living cells by using the
synthesizing machinery of the cell.
 Cause the synthesis of specialized
structures that can transfer the viral nucleic
acid to other cells.

FIGURE: Viruses and Bacteria Compared

Host Range
 The host range of a virus is the spectrum
of host cells the virus can infect.
 Viruses than infect bacteria are called
bacteriophages, or phages.
 For the virus to infect the host cell, the
outer surface of the virus must chemically
interact with specific receptor sites on the
surface of the cell.
 The use of bacteriophage to treat bacterial
infections is called phage therapy.
 Tumor destroying or oncolytic viruses may
selectively infect and kill tumor cells.

Viral Size
 Viral sizes are determined with the aid of
electron microscopy. Different viruses vary
considerably in size.
 Although most are quite a bit smaller than
bacteria, some of the larger viruses (such
as the vaccine virus) are about the same
size as some very small bacteria (such as
the mycomplasmas, rickettsias, and
chlamydias).
 Viruses range from 20 to 1000 nm in

FIGURE: Virus sizes. The sizes of several viruses (teal blue) and bacteria (pink)
are compared with a human red blood cell, shown to the right of the microbes.
Dimensions are given in nanometers (nm) and are either diameters or length by
width.

Viral Structure
 A virion is a complex, fully developed,
infectious viral particle composed of nucleic
acid and surrounded by a protein coat that
protects it from the environment and is a
vehicle of transmission from one host cell to
another.
 Viruses are classified by differences in the
structures of these coats.

FIGURE: Morphology of a nonenveloped polyhedral
virus. (a) A diagram of a polyhedral (icosahedral) virus. (b)
A micrograph of the odenovirus Mastadenovirus. Individual
capsomeres in the protein coat are visible.

Nucleic Acid
 A virus can have either DNA or RNA, but
never both.
 The nucleic acid of a virus can be single-
stranded or double-stranded. Thus, there
are viruses which the familiar double-
stranded DNA, with single-stranded RNA.
 Depending on the virus, the nucleic acid
can be linear or circular. In some viruses
(such as the influenza virus), the nucleic
acid is in several separate segments.

Capsid and Envelope
 The nucleic acid of a virus is surrounded by
a protein coat called the capsid.
 Each capsid is composed of protein
subunits called capsomers.
 In some viruses, the capsid is covered by
an envelope.
 Envelops may or may not be covered by
spikes.
 Viruses whose capsids are not covered by
an envelope are known as nonenveloped

FIGURE: Morphology of an enveloped helical virus. (a) A diagram
of an enveloped helical virus. (b) A micrograph of influenzavirus A2.
Notice the halo of spikes projecting from the outer surface of each
envelope.

FIGURE: Morphology of a helical virus. (a) A diagram of a portion of
a helical virus. Several rows of capsomeres have been removed to
reveal the nucleic acid. (b) A micrograph of Ebola virus, a flovirus
showing helical rods.

General Morphology
 Viruses may be classified into several
different morphology types on the basis of
their capsid architecture.
 The structure of these capsids has been
revealed by electron microscopy and a
technique called X-ray crystallography.

Helical Viruses
 Helical viruses resemble long rods that may
be rigid or flexible.
 The viral nucleic acid is found within a
hollow, cylindrical capsid that has a helical
structure.
 The viruses that care rabies and Ebola
hemorrhagic fever are helical viruses.

Polyhedral Viruses
 Many animal, plant, and bacterial viruses is
covered by an envelope.
 Enveloped viruses are roughly spherical.
When helical and polyhedral viruses are
enclosed by envelopes, they are called
enveloped helical or enveloped polyhedral
viruses.
 An example of an enveloped helical virus is
the Influenzavirus. An example of an
enveloped polyhedral (icosahedral) virus is

Complex Viruses
 Some viruses, particularly bacterial viruses,
have complicated structures and are called
complex viruses.
 One example of a complex virus is a
bacteriophage.
 Some bacteriophages have capsids to
which additional structures are attached.

FIGURE: Morphology of complex viruses. (a) A diagram and
micrograph of a T-even bacteriophage (b) A Orthopoxvirus, which
causes smallpox.

Taxonomy of Viruses
 The oldest classification of viruses is based
on symptomatology.
 Virologists began addressing the problem
or viral taxonomy in 1966 with International
Committee on the Taxonomy of Viruses
(ICTV).
 ICTV has been grouping viruses into
families based on:
1. Nucleic acid type
2. Strategy for replication

Taxonomy of Viruses
 The suffix – virus is used for genus names;
family names end in –viridae; and order
names end in – ales.
 In formal usage, the family and genus
names are used in the following manner:
Family Herpesviridae, genus
Simplexvirus, human herpes virus 2.

Taxonomy of Viruses
 A viral species is a group of viruses
sharing the same genetic information and
ecological niche (host range).
 Specific epithets for viruses are not used.
Thus, viral species are designated by
descriptive common names, such as
human immunodeficiency virus (HIV), with
subspecies (if any) designated by a number
(HIV – 1).

Isolation, Cultivation, and Identification of
Viruses
 Viruses must be provided with living cells
instead of a fairly simple chemical medium.
 Viruses that use bacterial cells as a host
(bacteriophages) are rather easily grown on
bacterial cultures.

FIGURE: Families of viruses that affect humans

Growing Bacteriophages in the Laboratory
 Bacteriophages can be grown either in
suspension of bacteria in liquid media or in
bacterial cultures on solid media.
 Solid media makes possible the plaque
method for detecting and counting viruses.
 A sample of bacteriophage is mixed with host
bacteria and melted agar.
 The agar containing the bacteriophages and
host bacteria is then poured into a Petri plate
containing a hardened layer of agar growth
medium.

Growing Bacteriophages in the Laboratory
 The virus-bacteria mixture solidifies into a
thin top layer that contains a layer of bacteria
approximately one cell thick.
 Each virus infects a bacterium, multiplies,
and releases several hundred new viruses.
 The newly produced viruses infect other
bacteria in the immediate vicinity, and more
new viruses are produced.
 This produces a number of clearings, or
plaques, visible against a lawn of bacterial
growth on the surface of the agar.

In Living Animals
 Animal inoculation may be used as a
diagnostic procedure for identifying and
isolating a virus from a clinical specimen.
 After the animal is inoculated with the
specimen, the animal is observed for signs of
disease, or is killed so that infected tissues
can be examined for the virus.

In Embryonated Eggs
 Growing viruses in an embryonated egg can
be a fairly convenient and inexpensive form
of host for many animal viruses.
 A hole is drilled in the shell of embryonated
egg, and a viral suspension or suspected
virus-containing tissue is injected into the
fluid of the egg.
 There are several membranes in an egg, and
the virus is injected near the one most
appropriate for its growth.

In Embryonated Eggs
 Viral growth is signaled by the death of the
embryo, by embryo cell damage, or by the
formation of typical pocks or lesions on the
egg membranes.
 This method was once the most widely used
method of viral isolation and growth, and it is
still used to grow viruses for some vaccines.

FIGURE: Inoculation of an embryonated egg. The injection site determines
the membrane on which the viruses will grow.

The Cell Cultures
 Cell cultures have replaced embryonated
eggs as the preferred type of growth medium
for many viruses.
 This cell deterioration is called cytopathic
effect (CPE), can be detected and counted in
much the same way as plaques caused by
bacteriophages on a lawn of bacteria.
 Primary cell lines, derived from tissue
slices, tend to die out after only a few
generations.

The Cell Cultures
 Contain cell lines, called diploid cell lines,
developed from human embryos can be
maintained for about 100 generations and
are widely used for culturing viruses that
require a human host.
 When viruses are routinely grown in the
laboratory, continuous cell lines are used.
These are transformed (cancerous) cells that
can be maintained through an indefinite
number of generations, and they are
sometimes called mortal cell lines.

FIGURE: Cell cultures. Transformed cells can be grown indefinitely in
laboratory culture.

Viral Identification
 Viruses cannot be seen without the use of an
electron microscope.
 Serological methods, such as Western
Blotting, are the most commonly used means
of identification. In these tests, the virus is
detected and identified by its reaction with
antibodies.
 Virologists can identify and characterize
viruses by using such modern methods as
restriction fragment length polymorphisms
(RFLPs) and the polymerase chain reaction

Viral Multiplication
 The nucleic acid in a virion contains only a
few of the genes needed for the synthesis of
new viruses. These include genes for the
virion’s structural components, such as the
capsid proteins, and genes for a few of the
enzymes used in the viral life cycle.
 These enzymes are synthesized and
functional only when the virus is within the
host cell.
 Thus, for a virus to multiply, it must invade a
host cell and take over the host’s metabolic

Multiplication of Bacteriophages
 Phages can multiply by two alternative
mechanisms; the lytic cycle or the lysonegic
cycle.
 The lytic cycle ends with the lysis and death
of the host cell, whereas the host cell
remains alive in the lysogenic cycle.

T - Even Bacteriophages; The Lytic Cycle
 The virions of T-even bacteriophages are
large, complex, and nonenveloped, with a
characteristic head-and-tail structure.
 The multiplication cycle of these phages, like
that of all viruses, occurs in five distinct
stages: attachment, penetration,
biosynthesis, maturation, and release.

FIGURE: The lytic cycle of a T-even bacteriophage

The Lytic Cycle
 Attachment. The first step of the lytic
process. During this process, an attachment
site on the virus attaches to a complementary
receptor site on the bacterial cell.
 Penetration. After attachment, the T-even
bacteriophage injects its DNA (nucleic acid)
into the bacterium. To do this, the
bacteriophage’s tail releases an enzyme,
phage lysozyme, which breaks down a
portion of the bacterial cell wall.

The Lytic Cycle
 Biosynthesis. Once the bacteriophage DNA
has reached the cytoplasm of the host
cell, the biosynthesis of viral nucleic acid and
protein occurs.
 Maturation. In the next sequence of
events, maturation occurs. Bacteriophage
DNA and capsule are assembled into
complete virions.
 Release. The final stage of viral multiplication
is the release of virions from the host cell.

Bacteriophage Lambda: The Lysogenic
Cycle
 Biosynthesis. Once the bacteriophage DNA
has reached the cytoplasm of the host cell,
the biosynthesis of viral nucleic acid and
protein occurs.
 Maturation. In the next sequence of events,
maturation occurs. Bacteriophage DNA and
capsule are assembled into complete virions.
 Release. The final stage of viral multiplication
is the release of virions from the host cell.

Bacteriophage Lambda: The Lysogenic
Cycle
 In lysogeny, the phage remains latent
(inactive). The participating bacterial host
cells are known as lysogenic cells.
 Some viruses do not cause lysis and death of
the host cell when they multiply.

FILE: The lysogenic cycle of bacteriophage in E. coli

Three results of Lysogeny:
 Fist, Immunity to reinfection by the same
phage.
 The second result of lysogeny is phage
conversion.
 The third result of lysogeny is that it makes
specialized transduction.

Multiplication of Animal Viruses
 Adsorption. The virus becomes attached to
the cells, and at this stage, it can be
recovered in the infectious form without cell
lysis by procedures that either destroy the
receptors or weaken their bonds to the
virions.
 Penetration. Rapidly follows adsorption, and
the virus can no longer be recovered from the
intact cell.

Multiplication of Animal Viruses
 Uncoating. The virus becomes attached to
the cells, and at this stage, it can be
recovered in the infectious form without cell
lysis by procedures that either destroy the
receptors or weaken their bonds to the
virions.
 Viral Nucleic Acid Replication. Virulent
viruses, either DNA and RNA, shut off cellular
protein synthesis and disaggregate cellular
polyribosomes, favouring a shift to viral

Comparison of Multiplication Cycles of Bacteriophage
and Animal Viruses
Stage Bacteriophage Animal Viruses
Attachment Tail fibers attach to cell wall
proteins
Attachment sites are plasma
membrane proteins and
glycoproteins
Penetration Viral DNA injected into host
cell
Capsid enters by endocytosis or
fusion
Uncoating Not required Enzymatic removal of capsid
proteins
Biosynthesis (Eclipse) In cytoplasm In nucleus (DNA viruses) or
cytoplasm (R.NA viruses)
Chronic infection Lysogeny Latency; slow viral infections;
cancer
Release Host cell lysed Enveloped viruses bud out;
nonenveloped viruses rupture
plasma membrane

FIGURE: The entry of
herpes simplex virus
(Simplexvirus) in an animal
cell. (a) Attachment of the
viral envelope to the plasma
membrane. (b) The cell’s
plasma membrane folds
inward, forming a vesicle
around the virus; this results
in loss of the envelope. (c)
The nonenveloped capsid
penetrates the cytoplasm of
the cell from the vesicle. (d),
(e), (f) The nucleic acid core is
uncoated by digestion of the
capsid.

The Biosynthesis of DNA Viruses
 Generally, DNA-containing viruses replicate
their DNA in the nucleus of the host cell by
using viral enzymes and they synthesize their
capsid and other proteins in the cytoplasm by
using host cell enzymes.
 Then the proteins migrate into the nucleus
and are joined with the newly synthesized
DNA to form virions.
 These virions are transported along the ER to
the host cell’s membrane for release.

FIGURE: Multiplication of Papovavirus, a DNA – containing
virus.

FIGURE: DNA-containing animal viruses. (a) Negatively stained adenoviruses that
have been concentrated in a centrifuge gradient. The individual capsomers are
clearly visible. (b) The envelope around this herpes simplex virus capsid has broken,
giving a “fried egg” appearance.

Some DNA viruses
 Adenoviridae. Named after adenoids, from
which they were first isolated, adenovirus
cause acute respiratory diseases – the
common cold.
 Poxviridae. All diseases caused by
poxviruses, including small pox and cowpox,
include skin lesions. Pox refers to pus-filled
lesions.
 Herpesviridae. Nearly 100 hepesviruses are
known. They are named after the spreading

Some DNA viruses
 Papovaviridae. Papovaviruses are named for
papillomas (warts), polymoas (tumors), and
vacuolation (cytoplasmic vacuoles produced
by some of these viruses). Warts are caused
by members of the genus Papillomavirus.
 Hepadnaviridae. Hepadnaviridae are so
named because they cause hepatitis and
contain DNA. The only genus in this family
causes hepatitis B.

The Biosynthesis of RNA Viruses
 The multiplication of RNA viruses is
essentially the same as that of DNA viruses,
except the several different mechanisms of
mRNA formation occur among different
groups of RNA viruses.
 RNA viruses multiply in the host cell’s
cytoplasm. The major difference among the
multiplication processes of these viruses lie
in how mRNA and viral RNA are produced.
Once viral RNA and viral proteins are

Some RNA Viruses
 Picornaviridae. Picornaviruses, such as
poliovirus, are single-stranded RNA viruses.
They are smallest viruses; and the prefix
pico- (small) plus RNA gives these viruses
their name.
 The RNA within the virion is called a sense
strand (or + stand), because it can act as
mRNA.
 After attachment, penetration, and uncoating
are completed, the single-stranded viral RNA

Some RNA Viruses
 Tagaviridae. Togaviruses, which include
arthropod-borne arboviruses or alphaviruses,
also contain a single + strand of RNA.
Togaviruses are enveloped viruses; their
name is from the Latin word for covering,
toga.
 Rhabdoviridae. Rhabdoviruses, such as
rabiesvirus (genus Lyssavirus), are usually
bullet-shaped. Rhabdo is from the Greek
word for rod, is not really an accurate

Some RNA Viruses
 Reoviridae. Reoviruses were named for their
habitats: the respiratory and enteric
(digestive) – systems of humans. Their name
comes from the first letters of
respiratory, enteric, and orphan.
 Retroviridae. Many retroviruses infect
vertebrates. One genus of
retrovirus, Lentivirus, includes the subspecies
HIV-1 and HIV-2, which cause AIDS.

FIGURE: Pathways of
multiplication used by
various RNA-containing
viruses. a) After uncoating,
ssRNA viruses with a +
strand genome are able to
sythesize proteins directly
from their + strand. Using the
+ strand as a template, they
transcribe – strands to
produce additional + strands
to serve as mRNA and be
incorporated into copied
proteins as the viral genome.
B) The ssRNA viruses with a
– strand genome must
transcrible a + strand to
serve as mRNA before they
begin synthesizing proteins.
The mRNA transcribes
additional strands for
incorporation into capsid
protein. Both ssRNA and (c)
dsRNA must use mRNA
(+strand) to code for
proteins, including capsid

Mutation and Cancer
 The first step in viral mutation is the
assembly of the protein capsid.
 The envelope protein is encoded by the viral
genes and is incorporated into plasma
membrane of the host cell.
 The envelope develops around the capsid by
a process called budding.
 After the sequence of
attachment, penetration, uncoating, and
biosynthesis or viral nucleic acid and
protein, the assembled capsid containing

Mutation and Cancer
 As a result, a portion of the plasma
membrane, now the envelope, adheres to the
virus.
 This extrusion of a virus from a host cell is
one method of release. Budding does not
immediately kill the host cell, and in some
cases the host cell survives.
 Nonenveloped viruses are released through
ruptures in the host cell plasma membrane.
In contrast to budding, this type of release
usually results in the death of the host cell.

Viruses and Cancer
 Several types of cancer are now known to be
caused by viruses. Molecular biological
research shows that the mechanisms of the
diseases are similar, even when a virus does
not cause cancer.
 The viral cause of cancer can often go
unrecognized because the particles of some
viruses infect cells but do not induce cancer.
Also, cancer might not develop until long
after viral infection. And cancers do not seem

The transformation of Normal Cells into
Tumor Cells
 Almost anything that can alter the genetic
material of a eukaryotic cell has the potential
to make a normal cell cancerous.
 These cancer-causing alterations to cellular
DNA affect parts of the genome called
oncogenes.
 Viruses capable of inducing tumors in animals
are called oncogenic viruses, or
oncoviruses.
 Tumor cells undergo transformation; they
acquire properties that are distinct from the

DNA Oncogenic Viruses
 Oncogenic viruses are found within several
families of DNA-containing viruses. These
groups Include the Adenoviridae,
Herpesviridae, Poxviridae, Papovaviridae,
and Hepadnaviridae.
RNA Oncogenic Viruses
 Among RNA viruses, only the oncoviruses in
the family Retroviridae cause cancer. The
human T-cell leukemia viruses (HTLV-1 and
HTLV-2) are retroviruses that cause adult T-
cell leukemia and lymphoma in humans.

Latent Viral Infections
 A virus can remain in equilibrium with the
host and not actually produce disease for a
long period, often many years.
 All of human herpesviruses can remain in
host cells throughout the life of an individual.
When the viruses are reactivated by
immunosuppression like AIDS, the resulting
infection may be fatal.
 An example of latent infection in viruses is
the infection of the skin by herpes semplex

Persistent Viral Infections
 A persistent viral infection is a disease
process that occurs gradually over a long
period caused by a virus.
 A persistent viral infection is different from a
latent viral infection in that detectable
infectious virus gradually builds over a long
period, rather than appearing suddenly.
 The measles virus is responsible for
persistent viral infections like sclerosing
panencephalitis (SSPE).

Prion Disease
 Other infectious diseases that have not been
found to have a viral cause might be caused
by prions. Such prion diseases include:
 Mad Cow Disease
 Scrapie
 Kuru
 Creutzfeldt–Jakob Disease (CJD)

All prion disease include:
 Involve neurodegeneration
 Are caused by proteins that misfold in the
brain
 Are also called Transmissible Spongiform
Encephalopathis (TSE)
- Mad cow disease is also known as
Bovine Spongiform Encephalopaty (BSE)

 These diseases are caused by the
conversion of a nomal host halogen into an
infectious form.
 The specific protein that misfolds during prion
disease is called PrP
 Normally found in membrane of cells
 Thought to play a role in normal transduction
 Normal form of PrP is Called PrPC (prion
protein, cellular form)
 Misfolded form of PrP is called PrPRes (prion
protein, resistant to enzyme degradation)
 A.k.a PrPSe (prion protein, scrapie form)
 Prion disease occurs when PrPC is

FIGURE: How a protein can be infectious. If an abnormal prion protein
(PrPSc) enters a call, it changes a normal prion protein to PrPSc which can
now change another normal PrP, resulting in an accumulation of the abnormal
PrPSc.

Resources:
Torota, Gerard J.; Funke, Berdell R.; Case
Christine .L; 2004. Introduction to
Microbiology; Viruses, Viroids, and Prions.
Pearson Edcuation Inc.
Cortan, Ramzi S.; Kumar, Vinay; Robbins,
Stanley L.; 1994. Pathologic Basis of
Disease 5th Edition, Infectious Diseases.
W.B Saunders Company.

Reporter:
Louis Carlo V. Lim
BS. Biology IV, Liceo de
Cagayan University
Virtual Assistant, Digital
Marketing Archive, San
Antonio TX
Instructor: Joy B. Pabillaran, Ph.D
Biology (on-going)

Microbiology - Noncellular Microbes - Louis Carlo Lim

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