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Examples of Cytopathic Effects of Viral Infection

• Nuclear shrinking (pyknosis) • Margination and breaking of chromosomes

• Proliferation of nuclear membrane • Rounding up and detachment of cultured cells

• Vacuoles in cytoplasm • Inclusion bodies

• Syncytia (cell fusion)

Quantitative Assays-TCID50

Tissue Culture Infectious Dose: TCID50 Measure cytopathic effects other than lysis

Concentration of virus it takes to produce cytopathic effect (CPE) in 50% of the dishes of cells

infected with virus (Table 2-2)(Figure 2-11)

B

A

Table( 2-2) Example of endpoint dilution data

Figure 2-10 example at cytopathic effect A-Inclusion bodies , BSyncytia

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Quantitative Assays

Plaque assays Lytic viruses only

• Steps Serial dilution of virion-containing solution

• Create tissue culture plates

• Spread diluted virus

• Overlay with agar—prevents diffusion

• Count number of plaques

• Each plaque represents 1 PFU (Plaque Forming Unit)(Figure 2-12)

Figure 2-12 plaque neutralization assay

Figure (2-11)

Endpoint

literation of

cytopathic effect

by tissue culture

assay

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Plaque forming Units

• A single virus infective dose can cause an area of cell destruction

• Movement of virus within cell is restricted by an agar overlay

• This causes areas of localized destruction

• Plaques are enumerated under a microscope to determine the plaque forming units per

ml (PFU/ml)

• This allows comparison of different viruses in the same unit

Calculation of PFU/mL(Figure 2-14)

Plaques are enumerated

Plaque Counts are averaged over wells

The average is then divided by the dilution times the volume

(𝟒𝟑 +𝟒𝟎 +𝟑𝟖)/𝟑

(𝟏𝟎 − 𝟒 × 𝟎. 𝟏)

= 𝟑, 𝟕𝟑𝟎, 𝟎𝟎𝟎 𝒑𝒇𝒖/𝒎𝒍

43 4 1 0

40 3 0 0

38 6 2 0

Plaques formed per well

Figure (2-12)Plaque forming units calculation

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Problems with cell culture

• Long period (up to 4 weeks) required for result.

• Often very poor sensitivity, sensitivity depends on a large extent on the condition of the

specimen.

• Susceptible to bacterial contamination.

• Susceptible to toxic substances which may be present in the specimen.

• Many viruses will not grow in cell culture e.g. Hepatitis B, Diarrhoeal viruses,

parvovirus, papillomavirus.

Hemadsorption Test

• Some viruses agglutinate RBCs Mumps, measles, influenza

• Haemagglutination Clumps RBCs (Figure 2-13)

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A

C

B

Figure (2-13)A-Haemagglutination assay (H) Principle of test B-Endpoint of Haemagglutination test CHaemagglutination of culture virus

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B

A

Figure(2-14)Direct Virological examination (A)Electron microscope (B)Principle of

immunofluorescence assay (C) immunofluorescence microscope.

C

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Polymerase Chain Reaction

 Advantages of PCR:

• Extremely high sensitivity, may detect down to one viral genome ( Figure 2-15) per

sample volume

• Easy to set up

• Fast turnaround time

 Disadvantages of PCR

• Extremely liable to contamination

• High degree of operator skill required

• Not easy to set up a quantitative assay.

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• A positive result may be difficult to interpret, especially with latent viruses such as

CMV, where any seropositive person will have virus present in their blood irrespective

whether they have disease or not.

 These problems are being addressed by the arrival of commercial closed systems such as

the Roche Cobas Amplicor which requires minimum handling. The use of synthetic

internal competitive targets in these commercial assays has facilitated the accurate

quantification of results. However, these assays are very expensive.

PCR - Polymerase Chain Reaction

PCR is an in vitro technique for the amplification of a region of DNA

 which lies between two regions of known sequence. (Figure 2-16)

PCR amplification is achieved by using oligonucleotide primers.

These are typically short, single stranded oligonucleotides which are complementary to the outer

regions of known sequence.

Figure (2-15 ) Structure of DNA

Figure(2-16) Two amplification regions of the DNA

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 The oligonucleotides serve as primers for DNA polymerase and the denatured strands of

the large DNA fragment serves as the template.

• This results in the synthesis of new DNA strands which are complementary to the parent

template strands.

• These new strands have defined 5' ends (the 5' ends of the oligonucleotide primers),

whereas the 3' ends are potentially ambiguous in length.

What is PCR? : (Figure2-17)

The “Reaction” Components

1. Target DNA - contains the sequence to be amplified

2. Pair of Primers - oligonucleotides that define the sequence to be amplified.

3. dNTPs - deoxynucleotidetriphosphates: DNA building blocks.

4. Thermostable DNA Polymerase - enzyme that catalyzes the reaction

5. Mg++ ions - cofactor of the enzyme

6. Buffer solution – maintains pH and ionic strength of the reaction solution suitable for

the activity of the enzyme

The Reaction:

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How Gel Electrophoresis of DNA Works

Figure(2-17)A-PCR equipment (B)Polymerase chain reaction steps

Figure(2-18)DNA gel electrophorese A-Equipment B-Principle assay

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Serology

Viral infection induce immune response the detection of rising titers of antibody between acute and

convalescent stages of infection, or detection of IgM in primary infection .(Figure 2-20)

Viral serology :

 Indirect

 Primary and secondary responses to viral infection

- IgM (1st exposure)

- IgG (2nd exposure)

Figure(2-19)Primary and secondary antibody responses toward a viral pathogen

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How useful a serological result is depends on the individual virus.

• For example, for viruses such as rubella and hepatitis A, the onset of clinical symptoms

coincide with the development of antibodies. The detection of IgM or rising titres of IgG

in the serum of the patient would indicate active disease.

• However, many viruses often produce clinical disease before the appearance of

antibodies such as respiratory and diarrhoeal viruses. So in this case, any serological

diagnosis would be retrospective and therefore will not be that useful.

• There are also viruses which produce clinical disease months or years after

seroconversion e.g. HIV and rabies. In the case of these viruses, the mere presence of

antibody is sufficient to make a definitive diagnosis.(Figure 2-21)

Figure (2-20)Principle of ELISA assay

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Problems with Serology:

• Long period of time required for diagnosis for paired acute and convalescent sera.

• Mild local infections such as HSV genitals may not produce a detectable humoral

immune response.

• Extensive antigenic cross-reactivity between related viruses e.g. HSV and VZV, Japanese

B encephalitis and Dengue, may lead to false positive results.

• immunocompromised patients often give a reduced or absent humoral immune

response.

• Patients with infectious mononucleosis and those with connective tissue diseases such as

SLE may react non-specifically giving a false positive result.

• Patients given blood or blood products may give a false positive result due to the

transfer of antibody.

CSF antibodies :

• Used mainly for the diagnosis of herpes simplex and VZV encephalitis

• CSF normally contain little or no antibodies

Figure(2-21)Microplate ELISA for HIV antibody: Coloured wells indicate reactivity

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• presence of antibodies suggest meningitis or

meningoencephalitis

𝑪𝑺𝑭 𝒂𝒏𝒕𝒊𝒃𝒐𝒅𝒚 𝒕𝒊𝒕𝒓𝒆

𝑺𝒆𝒓𝒖𝒎 𝒂𝒏𝒕𝒊𝒃𝒐𝒅𝒚 𝒕𝒊𝒕𝒓𝒆 >

𝟏

𝟏𝟎𝟎 𝒊𝒔 𝒊𝒏𝒅𝒊𝒄𝒂𝒕𝒊𝒗𝒆 𝒐𝒇 𝒎𝒆𝒏𝒊𝒏𝒈𝒊𝒕𝒊𝒔

• Diagnosis depends on the presence of an intact blood-brain barrier

What is blotting?

 Blots are techniques for transferring DNA , RNA and proteins onto a carrier so they can

be separated, and often follows the use of a gel electrophoresis. The Southern blot is used

for transferring DNA, the Northern blot for RNA and the western blot for

PROTEIN.(Figure 2-22)

Southern blotting

Professor Sir Edwin Southern, Professor of Biochemistry and Fellow of Trinity developed this

method in 1975.

Southern won the Lasker Award for Clinical Medical Research prize for the method of finding

specific DNA sequences he developed this procedure at Edinburgh University more than 30

years ago. The technique is known as DNA transfer or 'Southern blotting'

Figure (2-22)The three types of blotting techniques

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Southern Steps(Figure 2-24)( Figure 2-25)

1. DNA to be analyzed is digested to completion with a restriction endonuclease.

2. Electrophoresis to maximally separate restriction fragments in the expected size range. A set

of standards of known size is run in one lane of the gel.

3. Blot fragments onto a nitrocellulose membrane.

4. Hybridize with the 32P probe.

5. Autoradiography.

Figure (2-23) Professor Sir Edwin Southern

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Figure (2-24)Steps of southern blot technique

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Figure(2-25)General scheme for southern blot

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3. Herpesviruses

Properties of herpesviruses

• Enveloped double stranded DNA viruses.

• Genome consists of long and short fragments which may be orientated in either direction,

giving a total of 4 isomers.

• Three subfamilies:

A. Alphaherpesviruses - HSV-1, HSV-2, VZV

B. Betaherpesviruses - CMV, HHV-6, HHV-7

C. Gammaherpesviruses - EBV, HHV-8

• Set up latent or persistent infection following primary infection

• Reactivation are more likely to take place during periods of immunosuppression

• Both primary infection and reactivation are likely to be more serious in

immunocompromised patients.

Herpesvirus Particle

HSV-2 virus particle. Note that all herpesviruses have identical morphology and cannot be

distinguished from each other under electron microscopy.(Figure2-26)

Figure (2-26) Herpesvirus Particle

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Herpes Simplex Viruses

• Belong to the alphaherpesvirus subfamily of herpesviruses

• Double stranded DNA enveloped virus with a genome of around 150 kb

• The genome of HSV-1 and HSV-2 share 50 - 70% homology.

• They also share several cross-reactive epitopes with each other. There is also antigenic crossreaction with VZV.

• Man is the only natural host for HSV.

Epidemiology (1)

• HSV is spread by contact, as the virus is shed in saliva, tears, genital and other secretions.

• By far the most common form of infection results from a kiss given to a child or adult from a

person shedding the virus.

• Primary infection is usually subclinical in most individuals. It is a disease mainly of very

young children ie. those below 5 years.

• There are 2 peaks of incidence, the first at 0 - 5 years and the second in the late teens, when

sexual activity commences.

• About 10% of the population acquires HSV infection through the genital route and the risk is

concentrated in young adulthood.

Pathogenesis

• During the primary infection, HSV spreads locally and a short-lived viraemia occurs,

whereby the virus is disseminated in the body. Spread to the to craniospinal ganglia occurs.

• The virus then establishes latency in the craniospinal ganglia.

• The exact mechanism of latency is not known, it may be true latency where there is no viral

replication or viral persistence where there is a low level of viral replication.

• Reactivation - It is well known that many triggers can provoke a recurrence. These include

physical or psychological stress, infection; especially pneumococcal and meningococcal,

fever, irradiation; including sunlight, and menstruation.

Clinical Manifestations

HSV is involved in a variety of clinical manifestations which includes ;-

1. Acute gingivostomatitis

2. Herpes Labialis (cold sore)

3. Ocular Herpes

4. Herpes Genitalis

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5. Other forms of cutaneous herpes

7. Meningitis

8. Encephalitis

9. Neonatal herpes

Oral-facial Herpes

Acute Gingivostomatitis

• Acute gingivostomatitis is the commonest manifestation of primary herpetic infection.

(Figure 2-27)

• The patient experiences pain and bleeding of the gums. 1 - 8 mm ulcers with necrotic bases

are present. Neck glands are commonly enlarged accompanied by fever.

• Usually a self-limiting disease which lasts around 13 days.

Herpes labialis (cold sore)

• Following primary infection, 45% of orally infected individuals will experience reactivation.

The actual frequency of recurrences varies widely between individuals.

• Herpes labialis (cold sore) is a recurrence of oral HSV.

• A prodrome of tingling, warmth or itching at the site usually heralds the recurrence. About

12 hours later, red-ness appears followed by papules and then vesicles.

Figure (2-27)Gingivostomatitis

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Ocular Herpes

HSV causes a broad spectrum of ocular disease, ranging from mild superficial lesions

involving the external eye, to severe sight-threatening diseases of the inner eye. Diseases

caused include the following :

- Primary HSV keratitis – dendritic ulcers

- Recurrent HSV keratitis

- HSV conjunctivitis

Genital Herpes

• Genital lesions may be primary, recurrent or initial.

• Many sites can be involved which includes the penis, vagina, cervix, anus, vulva, bladder,

the sacral nerve routes, the spinal and the meninges. The lesions of genital herpes are

particularly prone to secondary bacterial infection eg. S.aureus, Streptococcus, Trichomonas

and Candida Albicans.

• Dysuria is a common complaint, in severe cases, there may be urinary retention.

• Local sensory nerves may be involved leading to the development of a radiculitis. A mild

meningitis may be present.

• 60% of patients with genital herpes will experience recurrences. Recurrent lesions in the

perianal area tend to be more numerous and persists longer than their oral HSV-1

counterparts.

Herpes Simplex Encephalitis

• Herpes Simplex encephalitis is one of the most serious complications of herpes simplex

disease. There are two forms:

• Neonatal – there is global involvement and the brain is almost liquefied. The mortality rate

approaches 100%.

• Focal disease – the temporal lobe is most commonly affected. This form of the disease

appears in children and adults. It is possible that many of these cases arise from reactivation

of virus. The mortality rate is high (70%) without treatment.

• It is of utmost importance to make a diagnosis of HSE early. It is general practice that IV

acyclovir is given in all cases of suspected HSE before laboratory results are available.

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Other Manifestations

• Disseminated herpes simplex are much more likely to occur in immunocompromised

individuals. The widespread vesicular resembles that of chickenpox. Many organs other than

the skin may be involved e.g. liver, spleen, lungs, and CNS.

• Other cutaneous manifestations include

- eczema herpeticum which is potentially a serious disease that occurs in patients with

eczema.

- Herpetic whitlow which arise from implantation of the virus into the skin and typically affect

the fingers.

- “zosteriform herpes simplex". This is a rare presentation of herpes simplex where HSV

lesions appear in a dermatomal distribution similar to herpes zoster.

Laboratory Diagnosis

1. Direct Detection

- Electron microscopy of vesicle fluid - rapid result but cannot distinguish between HSV and

VZV

- Immunofluorescence of skin scrappings - can distinguish between HSV and VZV

- PCR - now used routinely for the diagnosis of herpes simplex encephalitis

2. Virus Isolation

- HSV-1 and HSV-2 are among the easiest viruses to cultivate. It usually takes only 1 - 5 days

for a result to be available.

3. Serology

- Not that useful in the acute phase because it takes 1-2 weeks for before antibodies appear

after infection. Used to document to recent infection.

A-Cytopathic Effect of HSV in cell culture: Note the

ballooning of cells. (Linda Stannard, University of Cape

Town, S.A)

B-Positive immunofluorescence test for HSV antigen in epithelial

cell. (Virology Laboratory, New-Yale Haven Hospital(

A B

Figure (2-29)

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Management

At present, there are only a few indications of antiviral chemo-therapy, with the high cost of antiviral

drugs being a main consideration. Generally, antiviral chemotherapy is indicated where the primary

infection is especially severe, where there is dissemination, where sight is threatened, and herpes

simplex encephalitis.

Acyclovir – this the drug of choice for most situations at present. It is available in a number of

formulations:-

- I.V. (HSV infection in normal and immunocompromised patients)

- Oral (treatment and long term suppression of mucocutaneous herpes and prophylaxis of

HSV in immunocompromised patients)

- Cream (HSV infection of the skin and mucous membranes)

- Ophthalmic ointment

Famciclovir and valacyclovir – oral only, more expensive than acyclovir.

Other older agents – e.g. idoxuridine, trifluorothymidine, Vidarabine (ara-A).

• These agents are highly toxic and is suitable for topical use for opthalmic infection only

Varicella- Zoster Virus

Properties

• Belong to the alphaherpesvirus subfamily of herpesviruses

• Double stranded DNA enveloped virus

• Genome size 125 kbp, long and short fragments with a total of 4 isometric forms.

• One antigenic serotype only, although there is some cross reaction with HSV.

Epidemiology

• Primary varicella is an endemic disease. Varicella is one of the classic diseases of childhood,

with the highest prevalence occurring in the 4 - 10 years old age group.

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