School Science Lessons
Viruses
2024-07-10
Please send comments to: j.elfick@uq.edu.au
(UNBiology9)
Viruses
Contents
9.1 Viruses
9.2 Virus classification
9.3 Viruses and viral diseases
9.4 Bacteriophage
9.5 Coronavirus
9.6 Herpes, genital herpes, genital ulcers
9.7.0 Hepatitis
9.8.0 HIV/AIDS
9.9 Warts, genital warts
9.10 Zika virus
9.11 Virus diseases of plants
9.12 ToBRFV, New tomato virus, 19/02/2020
9.13 Tobamovirus
9.14 Virus list
9.1. Viruses
See 10.9.0: Sexually transmitted infections, STIs, genital diseases, contact tracing
1. A viruses contains DNA or RNA in a coat of protein.
The nucleic acid in the virus contains instructions for the cell to make new viruses.
A virus is a submicroscopic infectious agent that replication inside a cell by using the cell's own biochemical processes.
Viruses cause infected cells to produce progeny viruses.
Retroviruses use the enzyme reverse transcriptase to copy the viral RNA (ribonucleic acid) into DNA (deoxyribonucleic acid).
Viruses are not affected by antibiotics.
To transduce a cell is to transfer genetic material from another cell to that cell, another usually by a virus particle or a virus.
9.2 Virus classification
The classification of viruses can be based on the type and arrangement of the genetic material.
Group 1. dsDNA viruses, (e.g. Adenoviruses, Herpesviruses, Poxviruses) Double-strand DNA viruses include oral herpes, herpes zoster (shingles) genital herpes, chickenpox viruses, cold sore, Herpes simplex virus, types 1 and 2 (HSV-1 and HSV-2) Adenoviruses human adenoids, tonsils, Human Papilloma Virus (HPV) causes dermal warts and genital warts Condylomata acuminata, Molluscum Contagiosum Virus (dsDNA = a molecule of DNA consisting of two parallel strands joined by hydrogen bonds between complementary purines and pyrimidines; a double helix, the form in which DNA occurs in chromosomes).
Group 2. ssDNA viruses (+ strand or "sense"), (e.g. Parvoviruses)Single-strand DNA viruses include some of the smallest viruses (ssDNA = Single-Stranded DNA (Deoxyribonucleic Acid).
Group 3. dsRNA viruses, Double-strand RNA, (e.g. Reoviruses), include viruses responsible for diarrhoea in children.
Group 4. (+) ssRNA viruses (+ strand or sense), (e.g. Picornaviruses, Togaviruses), Single-strand RNA viruses include influenza, hepatitis A virus (HAV) infectious hepatitis from faecal contamination of food and water and possibly milk, shellfish, hepatitis C virus (HCV) from exchange of body fluid, blood transfusion, sexual contact, shared needles for intravenous drug use, severe acute respiratory syndrome (SARS) foot-and-mouth disease, yellow fever, rubella viruses and most plant viruses'.
Group 5. (-)ssRNA, (- strand or antisense) RNA, (e.g. Orthomyxoviruses, Rhabdoviruses) Single-strand RNA viruses include influenza, measles (rubeola) mumps infection of salivary glands (paramyxovirus) rabies, Ebola virus, foot-and-mouth disease.
Group 6. ssRNA-RT viruses (+ strand or sense), RNA with DNA intermediate in life cycle, (e.g. Retroviruses), Diploid single-strand RNA viruses that use reverse transcriptase, retroviruses, include HIV virus.
Group 7. ds DNA-RT viruses (e.g. Hepadnaviruses), Circular double-strand DNA viruses that use reverse transcriptase, include hepatitis B virus (HBV) serum hepatitis from exchange of body fluid, blood transfusion, sexual contact, pregnant mother to baby, shared needles for intravenous drug use.
Human Immunodeficiency Virus, HIV, and AIDS, is the acquired immune deficiency syndrome.
Infectious agent | Common name | Signs and symptoms
Junin virus | Argentine hemorrhagic fever | fever, headache, loss of appetite, vomiting, if left untreated: organ failure
BK virus | BK virus infection | usually asymptomatic; fever, difficulty urinating
Machupo virus | Bolivian hemorrhagic fever | headache, fever, myalgia, external and internal bleeding, convulsions, tremours
Sabiá virus | Brazilian haemorrhagic fever | flushing of face and chest, petechiae, bodily swelling caused by edema, low blood pressure
Chlamydia trachomatis | Chlamydia In women | if is not detected by their doctor, approximately half will develop pelvic inflammatory disease (PID)
Coxsackie B virus | Coxsackie B virus infection | fever, headache, sore throat, gastrointestinal distress, extreme fatigue as well as chest and muscle pain
Cytomegalovirus | Cytomegalovirus infection | fatigue, swollen glands, fever, sore throat, muscle aches
Parvovirus B19 | Erythema infectiosum (Fifth disease)
Human herpes virus 6 (HHV-6) and human herpes virus 7 (HHV-7) Exanthem subitum (Sixth disease)
Enteroviruses, mainly Coxsackie A virus and enterovirus 71 (EV71) Hand, foot and mouth disease (HFMD) | fever, rash, small blisters
Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) | Herpes simplex | blisters on genitalia and lips
Human papillomavirus (HPV) infection | Warts
Human parainfluenza viruses (HPIV) | Human parainfluenza virus infection
Human T-lymphotropic virus 1 (HTLV-1) | Human T-lymphotropic virus 1 infection
Epstein–Barr virus (EBV) | Epstein–Barr virus infectious mononucleosis (Mono)
Orthomyxoviridae species | Influenza (flu) | fever, chills, headaches, muscle pain or aching, a feeling of discomfort, loss of appetite, lack of energy/fatigue,
dry cough, sore or dry throat, hoarse voice, and a stuffy or runny nose.
Japanese encephalitis virus | Japanese encephalitis | fever, headache and malaise, cachexia, hemiparesis, convulsions body temperature between 38–41 °C<
JC virus | Progressive multifocal leukoencephalopathy | clumsiness, progressive weakness, and visual, speech, and sometimes personality changes
9.3 Viruses and viral diseases
1. Respiratory infections
Rhinovirus, (coronovirus), causes common cold, (Acute viral rhinopharyngitis; Acute coryza), nasal congestion, headache, sneezing, runny nose, sore throat.
Influenza, (orthomyxovirus), (influenza virus A, B, C), causes nasal obstruction, headache, sneezing, chest pain, cough.
Coronavirus disease 2019 (COVID-19), fever, cough, loss of taste and smell
SARS coronavirus causes Severe acute respiratory syndrome (SARS-CoV-2)
Respiratory syncytial virus (RSV) causes Respiratory syncytial virus infection, which may be a mild upper respiratory tract infections (URTI) or a severe lower respiratory tract infections (LRTI).
Adenovirus causes Adenovirus infection, fever, sore throat, conjunctivitis
Parainfluenza virus infection
2. Digestive system infections
Gastrointestinal viral diseases, spread by ingestion into the digestive tract, cause gastroenteritis.
Norovirus infection, Rotavirus infection, Adenovirus infections, Astrovirus infection, diarrhoea, nausea, vomiting, fever, abdominal pain.
Hepatitis viruses cause liver disease.
3. Eruptive viral diseases, rash causing viruses, spread from skin contact
Varicella zoster virus, (VZV), causes Chickenpox, (and shingles), nausea, loss of appetite, aching muscles, headache, chickenpox rash.
Alphavirus Chikungunya causes Chikungunya, transmitted by Aedes Aegypti mosquito, high fever, severe joint pain, rash.
Fifth disease, caused by parvovirus.
Measles virus | Measles Fever, (rubeola, subacute sclerosing panencephalitis), cough, runny nose, inflamed eyes, rash and Koplik's spots.
Rubella virus | Rubella, (German measles), now regional elimination.
Monkeypox virus | Monkeypox Fever, with headache, muscle pains, shivering, blistering rash, swollen lymph nodes
Variola major or Variola minor viruses | smallpox, which has been eradicated worldwide, but some cultures exist in laboratories.
4. Hepatic viral diseases, (liver inflammation diseases)
9.7.0 Hepatitis
5. Cutaneous viral diseases, spread through physical contact
Warts, Genital warts, Human Papilloma Virus (HPV), Genital warts, (Condyloma acuminata)
Variola major or Variola minor
Varicella zoster virus (VZV) Shingles (Herpes zoster)
9.6 Herpes, genital herpes, genital ulcers
9.5 Herpes, Oral herpes, Genital herpes
Molluscum contagiosum virus (MCV) causes Molluscum contagiosum (MC, small raised, pink lesions with a central dimple
6. Viral haemorrhagic fevers
Haemorrhagic viral diseases
Crimean-Congo hemorrhagic fever virus causes Crimean-Congo hemorrhagic fever (CCHF)
Dengue fever viruses, (DEN-1, DEN-2, DEN-3 and DEN-4) cause Dengue Fever, transmitted by Aedes Aegypti mosquito, high fever, flu-like symptoms, muscle and joint pains, and a rash, if severe then dengue hemorrhagic fever.
Ebola virus disease from body fluids of infected animals.
Lassa virus causes Lassa fever, partial or complete hearing loss.
Marburg virus causes Marburg Haemorrhagic Fever (MHF), fever, weakness.
Yellow fever virus causes Yellow Fever, from infected mosquitoes.
7. Neurologic viral diseases
Nipah virus causes Nipah virus infection, diarrhoea, vomiting, stomach pain, headache.
Mumps virus, (Paramyxovirus) causes Mumps, fever, headache, malaise, muscle pain, and loss of appetite
Poliovirus caused Poliomyelitis Fever, which attacked motor neurones, paralysis and atrophy of muscles, but now worldwide eradication.
Rabies lyssavirus caused Rabies Fever, infected peripheral nerves then central nervous system, with extreme aversion to water, excessive salivary secretion, hallucinations, but worldwide elimination in humans and animals.
Viral meningitis, Viral encephalitis
West Nile virus causes West Nile fever, transmitted by mosquitoes, joint pain and skin rash.
8. Congenital virus infections
Cytomegalovirus (CMV) a herpes virus causes congenital CMV, now regional elimination
,
Rift Valley fever virus causes Rift Valley fever (RVF), affects grazing animals which may infect humans, causing mild fevers.
9.10 Zika virus
9. Sexually transmitted viruses
9.8.1 HIV/AIDS, weakens the immune system
HPV (Human Paoillomavirus), may cause cervical cancer
Genital herpes, Herpex simplex, HSV-1, HSV-2
Hepatitus B, causes liver inflammation
9.4 Bacteriophage
See diagram 9.3.70: T4 bacteriophage that attacks E. coli.
A bacteriophage or "phage" is a very small virus that infects bacteria.
The T4 bacteriophage infects the bacterium Escherichia coli, E.coli, found in the human gut.
This infection is used to study viruses and how they infect and replicate inside cells.
T-phages have head, capsid, containing double-stranded DNA genetic material.
The tail of the bacteriophage includes the tail, sheath, base plate and tail fibres, made of different proteins, used to attach itself to the bacterium.
The phage then inserts its own genetic material inside of the host bacterial cell so that it replicates and make more bacteriophages.
9.5 Coronavirus
COVID-19 virus Centres for Disease Control and Prevention
CORONAVIRUS National Institutes of Health
Coronaviruses are a big group of viruses that cause illnesses such as the common cold or more recent diseases including SARS (severe acute respiratory syndrome) and MERS.
COVID-19, (Corona Virus Disease 19), is a new strain that has not been previously identified in humans.
The viruses are named for the corona, or crown, of surface proteins that the virus uses to penetrate the cells of its host.
Coronavirus disease 2019
(COVID-19) is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2, (SARS-CoV-2).
The disease had spread globally by 13/03/2020, since 2019, resulting in the 2019–20 coronavirus pandemic.
Common symptoms include fever, cough and shortness of breath.
Muscle pain, sputum production and sore throat are some of the less common symptoms.
While the majority of cases result in mild symptoms, some progress to pneumonia and multi-organ failure.
The case fatality rate is estimated at between 1% and 5%, but varies by age and other health conditions.
Kill Coronavirus by washing your hands with soap.
Based on article by Palli Thordarson, Professor of Chemistry, University of New South Wales.
Viruses can be active outside the body for hours, even days.
Disinfectants, liquids, wipes, gels and creams containing alcohol are all useful at getting rid of them, but they are not quite as good as normal soap.
Health authorities have been giving us two messages:
1. When you have the virus there are no drugs that can kill it or help you get rid of it.
2. Wash your hands to stop the virus spreading.
Why does soap work so well on the Coronavirus, and indeed most viruses?
Because the virus is a self-assembled nanoparticle in which the weakest link is the lipid (fatty) bilayer.
Soap dissolves the fat membrane and the virus falls apart and dies, or rather, we should say it becomes inactive as viruses aren’t really alive.
Most viruses consist of three key building blocks: ribonucleic acid (RNA), proteins and lipids.
A virus-infected cell makes lots of these building blocks, which then spontaneously self-assemble to form the virus.
There are no strong covalent bonds holding these units together, so you do not necessarily need harsh chemicals to split those units apart.
When an infected cell dies, all these new viruses escape and go on to infect other cells.
Some end up also in the airways of lungs.
When you cough, or especially when you sneeze, tiny droplets from the airways can fly up to 10 metres.
The droplets are thought to be the main Coronavirus carriers and they can go at least two metres.
These tiny droplets end on surfaces and often dry out quickly, but the viruses remain active.
Human skin is an ideal surface for a virus, because it is “organic” and the proteins and fatty acids in the dead cells on the surface interact with the virus.
When you touch, say, a steel surface with a virus particle on it, it will stick to your skin and hence get transferred on to your hands.
If you then touch your face, especially your eyes, nostrils or mouth, you can get infected, and most people touch their face once every two to five minutes.
Washing the virus off with water alone might work, but water is not good at competing with the strong, glue-like interactions between the skin and the virus.
Soapy water is different, because it contains fat-like substances, amphiphiles, some of which are structurally similar to the lipids in the virus membrane.
An amphiphile chemical compound, (Greek amphis, philia both love), has both hydrophilic (water-loving) and lipophilic (fat-loving) properties.
The soap molecules “compete” with the lipids in the virus membrane, which is similar to how soap also removes normal dirt from the skin.
The soap not only loosens the “glue” between the virus and the skin, but also the Velcro-like interactions that hold the proteins, lipids and RNA in the virus together.
Coronavirus hits ill and disabled people hardest.
Alcohol-based products, including most “disinfectant” products, contain typically 60-80% ethanol, and kill viruses in a similar fashion.
But soap is better, because you only need a fairly small amount of soapy water, which, with rubbing, covers your entire hand easily.
Whereas you need to literally soak the virus in ethanol for a brief moment, and wipes or rubbing a gel on the hands does not guarantee that you soak every corner of the skin on your hands effectively enough.
Soap is the best, but do use alcohol-based sanitisers, when soap is not handy or practical.
9.6 Herpes, genital herpes, genital ulcers
Genital herpes is caused by herpes viruses.
Encephalitis, caused by the Herpes Simplex virus, causes headache, fever, inflammation of the brain, carried by mosquitoes, eastern equine encephalitis is fatal.
The herpes simplex virus can cause "cold sores" if the mouth is infected or genital ulcers if the sexual organs are infected.
The symptoms include clusters of small painful blisters that become ulcers then in two weeks.
People infected with the herpes virus may never develop any symptoms and so remain unaware of the infection.
The first infection of genital herpes has usually the worst symptoms.
The symptoms may recur when people are tired or tense or never recur.
If a person has genital herpes, the virus in specific nerve cells and may be passed on by sexual contact, even if the infected person does not have an outbreak of herpes blisters or ulcers.
There is no cure for herpes. but it can be managed to ease the symptoms by bathing the sores in saltwater.
An ice block wrapped in a towel may stop blisters forming.
A viral STD, herpes comes in two common strains, HSV1 and HSV2. HSV1 is the herpes cold sore virus, a variety that is common to see around the mouth, while HSV2 is most often associated with genital sores.
Symptoms: Collection of small white bumps clumped on the external genitalia, or in the pubic region.
Single large puss-like pustules may form along with scabbing over of the infected area.
Treatment: Herpes is treated with antiviral drugs, but the virus cannot be cured.
People with the herpes virus need to know that they can transmit the virus even when they do not have any sores or other symptoms.
Because the virus lives in the nerve endings, a reduction in stress and intense rubbing will prevent further outbreaks.
Sleep is also a powerful treatment.
HSV-1 (Herpes simplex 1)
HSV-1, herpes simplex virus causes cold sores, painful blemishes of the mouth (fever blisters).
It can become dormant for years, when drugs cannot affect it
Years later, it can be revived by excessive sunlight or fever to cause a cold sore in the same place as before.
HSV-2 (Herpes simplex 2)
HSV-2 causes painful genital sores that can return late in life as shingles.
The Herpes varicella-zoster virus causes chicken pox (varicella) in the skin of children as red spots that become small bubbles then become dry crusts.
In adults, the Herpes varicella-zoster virus causes shingles (zoster) as painful lesions in a pattern along the sensory nerves.
5.9.3 Herpes, genital herpes, genital ulcers
Herpes contact tracing, Herpes simplex viruses
Genital herpes is caused by herpes viruses.
The herpes simplex virus can cause "cold sores" if the mouth is infected or genital ulcers if the sexual organs are infected.
The symptoms include clusters of small painful blisters that become ulcers then in two weeks.
People infected with the herpes virus may never develop any symptoms and so remain unaware of the infection.
The first infection of genital herpes has usually the worst symptoms.
The symptoms may recur when people are tired or tense or never recur.
Once a person has genital herpes, the virus stays in specific nerve cells and may be passed on to other people by sexual contact, even if the infected person does not have an outbreak of herpes blisters or ulcers.
There is no cure for herpes. but it can be managed to ease the symptoms by bathing the sores in saltwater.
An ice block wrapped in a towel may stop blisters forming.
A viral STD, herpes comes in two common strains, HSV1 and HSV2. HSV1 is the herpes cold sore virus, a variety that is common to see around the mouth, while HSV2 is most often associated with genital sores.
Symptoms: Collection of small white bumps clumped on the external genitalia, or in the pubic region.
Single large puss-like pustules may form along with scabbing over of the infected area.
Treatment: Herpes is treated with antiviral drugs, but the virus cannot be cured.
People with the herpes virus need to know that they can transmit the virus even when they do not have any sores or other symptoms.
Because the virus lives in the nerve endings, a reduction in stress and intense rubbing will prevent further outbreaks.
Sleep is also a powerful treatment.
9.7.0 Hepatitis
9.7.1 Hepatitis A, Nausea, vomiting, diarrhea, dark urine, jaundice, fever, abdominal pain
9.7.2 Hepatitis B, yellowish skin, tiredness, dark urine, abdominal pain
9.7.3 Hepatitis C, no symptoms, needs blood testing
Hepatitis D Virus causes Hepatitis D, tired, nausea and vomiting.
Hepatitis E virus causes Hepatitis E, nNausea, jaundice.
9.7.1 Hepatitis A
Causative organism: Hepatitis A virus
Hepatitis A is transmitted by the faecal-oral route.
This may be food- or water-borne or via sexual contact, particularly between men.
Incubation period: 1550 days (mean 28 days)
How far back to trace 50 days from onset of symptoms
Usual testing method: Serology for hepatitis A (Hepatitis A IgM positive
Common symptoms: Acute hepatitis with jaundice, malaise, abdominal pain, dark urine
Likelihood of transmission per act of unprotected intercourse: Probably high if any faecal contamination of mouth
Likelihood of long-term sexual partner being infected: High, if susceptible
Protective effect of condoms: Nil (transmission is faecal-oral)
Transmission by oral sex: Possible if faecal contamination is present
Duration of potential infectivity: Two weeks before the onset of jaundice to one week after
Important consequences: Rarely, severe hepatitis and acute liver failure
Direct benefit of detection and treatment of contacts: Passive and active immunization against hepatitis A
Usual management of contacts: Passive immunization with human immunoglobulin 2.0 mL by intramuscular injection within 2 weeks of exposure.
Start active vaccination course immediately
Contact tracing priority: High: including sexual contacts, domestic contacts, close social contacts, and food handlers
Notification: Acute viral hepatitis A is notifiable by all doctors and laboratories in all Australian states and territories, and New Zealand.
If locally acquired, telephone a public health unit within 24 hours.
9.7.2 Hepatitis B
See 5.1.7: Hepatitis B contact tracing, Hepatitis B virus
This disease is caused by is a virus that affects the liver.
The virus is spread by blood to blood contact, e.g. sharing needles, or by sexual intercourse, vaginal, oral or anal.
People who are infected may have no symptoms at all or they may become ill with fever, nausea, dark urine or jaundice, yellow skin and eyes.
After infection, most adults recover, develop antibodies to the virus and cannot spread the virus to others.
A few people retain the virus, become carriers, may infect other people, and have an increased risk of developing liver disease.
A vaccine for Hepatitis B is available.
It is not effective for Hepatitis B carriers.
Vaccination for hepatitis B - Getting vaccinated for Hepatitis B is not something that everyone thinks about.
Immunize is a site that helps you answer the big question, should I get vaccinated?.
9.7.3 Hepatitis C
See 5.1.8: Hepatitis C contact tracing, Hepatitis
C virus
This disease is caused by another virus that affects the liver.
At this stage, there is no test to show whether a person has completely
cleared the virus from the body or if the person remains a
carrier and can infect others.
It is suspected that more people remain carriers than with Hepatitis B
disease, long-term carriers may develop liver problems years after infection.
Hepatitis C is spread by blood to blood contact.
It does not appear to spread easily by sexual contact.
Currently, it would appear that many patients with Hepatitis C have been
infected by sharing needles or other drug using equipment or
by infected blood transfusions.
In some countries, blood is routinely screened for Hepatitis C before transfusion.
In 2006 there is no vaccine available for Hepatitis C disease.
People with Hepatitis C disease should be checked by a doctor every few
years.
Significant advances have recently, 2013, been made in the management of
hepatitis C virus (HCV).
These advances include the use of non-invasive methods to assess liver
fibrosis, interleukin 28B genotype testing to predict interferon responsiveness and the use of new antiviral regimens for HCV
genotype
I, using antiviral agents (boceprevir and telaprevir).
These protease inhibitors are used in combination with pegylated interferon
and ribavirin as triple therapy for genotype I HCV.
The protease inhibitors are the first of many antiviral drugs to become
available to treat HCV, heralding the arrival of new agents that
will offer greater chances of cure with improved safety and tolerability
compared with current therapies.
5.1.7 Hepatitis B
Causative organism: Hepatitis B virus
Incubation period: 45180 days (mean 60 days)
How far back to trace 6 months prior to onset of acute symptoms
Usual testing method: Serology for hepatitis B (hepatitis B surface antigen positive)
Common symptoms: Jaundice, malaise, abdominal pain, dark urine
Likelihood of transmission per act of unprotected intercourse: Unknown
Likelihood of long-term sexual partner being infected: >20%
Protective effect of condoms: High
Transmission by oral sex: Low
Duration of potential infectivity: Two weeks before onset of symptoms and until the patient becomes surface antigen negative; lifelong if chronic infection
Important consequences: Severe, acute hepatitis, chronic liver disease, cirrhosis and liver cancer
Direct benefit of detection and treatment of contacts: Vaccination against hepatitis B or detection and management of hepatitis B infection
Usual management of contacts: Counselling and testing (up to 12 weeks after exposure).
Active vaccination against hepatitis B (3 injections over 6 months), or accelerated regime at 0, 1 and 3 months.
If high risk of transmission, seek further medical treatment.
Contact tracing priority:
High for sexual contacts, needle-sharing contacts, a newborn child of an infected mother, and household and close contacts if any risk exposures
Notification:
Acute viral hepatitis B is notifiable by doctors in all Australian states and territories, and New Zealand.
Hepatitis B surface antigen-positive results must be notified by laboratories in NSW.
Note: Hepatitis D virus (delta agent) is a deficient virus that is entirely dependent on concurrent Hepatitis B infection.
Measures to control Hepatitis B should control HDV.
5.1.8 Hepatitis C
Causative organism: Hepatitis C virus
Incubation period: Up to several months for acute infection
How far back to trace 6 months prior to onset of acute symptoms; if asymptomatic according to risk history
Usual testing method: Serology for hepatitis C, hepatitis C polymerase chain reaction (PCR) test to confirm persistent infection through detection of circulating viral RNA
Common symptoms: Most people experience no symptoms
Some people may have acute hepatitis with nausea, dark urine, jaundice, abdominal discomfort, fatigue
Likelihood of transmission per act of unprotected intercourse: Sexual transmission of Hepatitis C is controversial.
The likelihood of transmission via sex is generally low.
However, there have been reports of sexual transmission between HIV positive MSM
Likelihood of long-term sexual partner being infected: <5% (if no other risk factors)
Protective effect of condoms: Unknown
Transmission by oral sex: Probably rare
Duration of potential infectivity: Unknown, but possibly lifelong; increased if high viral load.
PCR-negative people appear to be non-infectious
Important consequences: Severe hepatitis, chronic liver disease, cirrhosis and liver cancer
Direct benefit of detection and treatment of contacts: Hepatitis C-infected partners should be monitored and managed and may respond to treatment
Usual management of contacts: Counselling and testing (antibodies may take up to 6 months to develop)
Contact tracing priority: High for needle-sharing contacts, blood donors and recipients.
High for children born to an infected mother.
Low for sexual contacts.
Notification: Acute viral hepatitis C is notifiable by all doctors in all Australian states and territories, and New Zealand
If the index patient has received or donated blood within 6 months of developing symptoms, also advise the relevant blood bank.
9.8.0 HIV/AIDS
9.8.1 Human Immunodeficiency virus, (HIV)
9.8.2 Causes of infection by the Human immunodeficiency virus (HIV)
9.8.3 Description of infection by HIV
9.8.4 Diagnosis of HIV/AIDS
9.8.5 Symptoms of HIV/AIDS
9.8.6 Treatment of HIV/AIDS
9.8.7 The effects of HIV/AIDS
9.8.8 The ABC of protection against HIV and the development of AIDS
9.8.1 Human immunodeficiency virus, (HIV)
HIV (Human immunodeficiency virus) AIDS (acquired immunodeficiency syndrome) Opportunistic infections
Acquired Immunodeficiency Syndrome, AIDS
The acquired immunodeficiency syndrome, AIDS, is a range of medical conditions, a syndrome, that occurs when a person's immune system is seriously weakened by infection from the human immunodeficiency
virus, HIV.
So there is no such thing as an "AIDS virus".
HIV is called a retrovirus, because it can change its own RNA (ribonucleic acid) genetic material into DNA (deoxyribonucleic acid) to cause the host cell's DNA to produce more HIV.
Blood contains three types of cells, erythrocytes, thrombocytes, and leucocytes.
Leucocytes, white blood cells, are responsible for the defence of the body against disease.
One type of white cell, the T-lymphocyte, T-helper cell, is essential for immunity, because it recognizes foreign antigens from its memory of previous infections and alerts other white cells to destroy the foreign
antigen.
HIV attacks the T-helper cells, reproduces inside them and kills them, causing a gradual deterioration of immune functions following the initial HIV infection.
A person with not enough T-helper cells to respond to infection will become ill and develop AIDS.
The infected person loses resistance to diseases and may die of opportunistic infections or AIDS-related illnesses, e.g. tuberculosis or bronchitis.
The opportunistic infections that occur in a person infected with HIV are caused first by destruction of immune defences by the virus and secondly by infections in your everyday environment.
These infections can often be treated, but there is no successful treatment for the immune deficiency caused by the virus.
9.8.2 Causes of infection by the Human Immunodeficiency Virus (HIV)
HIV is the virus that causes AIDS, and is transmitted through the exchange of bodily fluids; semen, vaginal secretions, breast milk and blood.
Infection can occur from any activity that allows body fluids infected with HIV to enter the bloodstream through a break in the skin, e.g. a cut or open sore.
Body fluids include blood, menstrual blood, bleeding gums, semen, vaginal secretions, breast milk, amniotic fluid, and pre-ejaculate.
Infection can occur in the following circumstances:
1. Unprotected sexual contact with an infected person, i.e. sexual intercourse without using a condom.
The virus can enter the body through the lining mucosa of the vagina, penis and rectum, especially if these linings are already damaged by STIs that cause ulcers or inflammation.
2. Using needles and / or syringes drug injections contaminated with minute quantities of blood containing the virus.
3. Transfusion of infected blood or blood clotting factors.
This should not occur when blood is properly screened in hospitals for HIV antibodies.
4. Babies being born to HIV-infected mothers becoming infected before or during birth or through breast feeding.
5. Cutting the skin without sterilizing between persons, e.g. tattooing, piercing, circumcision, female genital cutting.
There is no scientific evidence to support transmission of AIDS by mosquitoes, shaking hands, drinking from the same glass, sharing clothes, sitting on toilet seats, swimming, hugging, or looking after AIDS-positive
adults or children living with AIDS.
9.8.3 Description of infection by HIV
After infecting a new host, HIV starts rapidly reproducing itself inside the host's cells to produce new viruses that infect additional cells.
The viral replication may be so intensive that within a month after infection the infected individuals may have 100 million viral copies per mL of blood plasma.
The first line of natural immune defence is the non-specific immune system consisting of cells that patrol the body to destroy any virus-infected cell they encounter.
However, in most HIV-infected individuals the non-specific immune system may be overwhelmed by the initial onslaught of replicating HIV.
However, antigen presenting cells of the non-specific immune system engulf some viral proteins so that they can later show them to more specialized immune system components with the aim of producing a specify response to the HIV.
The antigen presenting cells include the helper T cells and killer T cells.
When the killer Y cells have received a description of the infecting virus intruder and a chemical signal from helper T cells, they multiply, then start destroying the infecting virus approximately three weeks after the initial infection.
The killer T cells do destroy most virus-infected cells and drive down the virus levels.
However, usually the response is not enough to prevent lifelong chronic infection.
The helper T cells direct the activities of other immune cells, but from the start of the infection, the HIV infects helper T cells themselves to replicate inside them and destroying them.
The HIV destroys the "memory helper" T cells that hold the immune system's memory of past exposures to pathogens.
A few weeks after the initial infection, so many memory helper T cells are destroyed that the control of the immune system is destroyed and never fully recovers.
Meanwhile, the HIV has a method of evading the killer T cells.
After entering a cell, the HIV copies its RNA genetic material into DNA in an inexact procedure that result in mutations in the viral copy.
These mutations are passed to the next generation every time the next generation of viruses copy themselves.
Also, if two viruses infect the same cell, they can swap genetic material by recombination and produce another virus variant for the next generation.
The increasing genetic diversity of HIV proteins causes them to become increasingly unrecognizable to immune cells that can only remember the original version of the virus.
As the killer T cells destroy all the cells displaying recognizable antigens, the virus-infected cells carrying mutant proteins take over.
Similarly, the antibodies produced by the immune system, weeks after the initial infection cannot recognize many of the HIV proteins in the host later in the infection.
Immune defences are usually unable to recognize variant versions of HIV.
So even a strong vaccine-evoked memory response against one strain of HIV might be ineffective against the strain that later enters the body or might become useless as the virus mutates.
HIV mutates so rapidly that the diversity of proteins on the surface of HIV particles in a single person after six years of infection is estimated to be greater than the diversity of all the human flu viruses strains world wide in a given year.
9.8.4 Diagnosis of HIV/AIDS
You cannot tell just by looking if someone is infected with HIV, because some HIV positive people can stay healthy and look healthy
for many years.
A person who has the HIV infection has antibodies in the blood to the virus
but may not have developed any of the illnesses of AIDS.
The only sure way of knowing is to get tested with the ELISA blood tests
then confirm the result with the Western blot blood tests.
Also, saliva tests are used.
Voluntary testing for HIV before marriage is recommended.
Antibodies are proteins that attack and remove any foreign organisms and
toxins, antigens, in the blood.
HIV is an antigen.
The antibodies produced by HIV infection cannot get rid of it. but the existence
of "marker" antibodies show that HIV infection has
occurred.
Receiving pre-test and post-test counselling is important.
People may be infected without knowing it and transmit HIV to others during
this time.
However, the tests that identify the antibodies to HIV usually give a negative
result for the first one to three months after initial infection,
called the "window period".
So a person who has been at risk of recent infection who receives a negative
test result should get a repeat of the test after three to four
months.
Counselling should be given before and after the tests to ensure that the
patient understands the implications of either a positive or
negative result.
The doctor should give the test results face-to-face and ensure that all
information about the test remains confidential.
9.8.5 Symptoms of HIV/AIDS
Symptoms include fever, fatigue and flu-like symptoms.
Weight loss and skin rashes along with pneumonia are also common symptoms.
As the virus continues to attack the immune system, a person will develop symptoms of the disease, e.g. persistent fatigue, swollen lymph glands, rapid weight loss, night sweats, memory loss, persistent diarrhoea.
When the immune system is severely damaged, certain cancers, infections
and brain disorders can occur.
For example, the appearance of purple blotches on the skin may indicate
Kaposi's Sarcoma (KS).
This stage of the illness is called AIDS.
9.8.6 Treatment of HIV/AIDS
In 2022, HIV infection can be treated. but not cured, because the body cannot rid of it.
However, there are many medications, called antiretroviral therapy (ART), that can control HIV and prevent complications.
There are three types of treatment that can be very effective if early
diagnosis occurs:
1. Antiretroviral medication is used to slow the reproduction of the virus
but not cure AIDS.
There is no such thing as an "AIDS vaccine".
HIV targets the immune system and it is a retrovirus that can insert itself
into the genetic material, replicate quickly and often mutate.
The first anti-HIV drug, AZT, was licensed in 1987.
It inhibits the HIV enzyme reverse transcripts that the virus uses to convert
its single strand of RNA into double strand DNA before splicing itself into
the genome of the host cell.
However, the high rate of mutation by the HIV virus allowed resistance
to the drug to develop.
So medical researchers developed many other "antiretroviral" drugs to
be taken in different combinations, e.g. Lamivudine, Viread and Ziagen.
Other types of anti-HIV drugs are the following:
1.1 Fusion inhibitors (entry inhibitors), e.g. Enfuvirtide, that interferes
with the HIV ability to enter cells.
1.2 Integrase inhibitors, e.g. Raltegravir, that block the enzyme integrase that the HIV virus uses to integrate its genetic material into the host cell's DNA.
1.3 Maturation inhibitors, e.g. Bevirimat, that block replication of the
HIV virus.
HIV positive patients living in countries where these drugs are available
and who have a healthy lifestyle and can afford the treatment
have lived an almost normal lifestyle for over 15 years since the initial infection.
2. The opportunistic infections and AIDS-related illnesses can be treated
with medications.
3. AIDS is a life threatening illness. but people with HIV can improve their
lifestyle to help them live healthy lives for many years.
AIDS is more likely to be appear when the person suffers from other infections,
drug and alcohol abuse, poor nutrition, and stress.
All the medications must be taken together and consistently.
Current drug regimens can suppress HIV. but no treatments can completely
eliminate the virus from the patient's body, because places
where the virus can hide are still being discovered.
4. Most people with HIV are treated with a combination of drugs known as
highly active antiretroviral therapy, or HAART.
These can include NRTIs (Nucleoside Reverse Transcriptase Inhibitors) which
are the drug cocktails that many people refer to when thinking of HIV.
5. In South Africa, the pre-exposure prophylaxis tablet PrEP, "Truvada",
is prescribed for HIV negative patients exposed to the virus,
e.g. female students between 15 and 24 and commercial sex workers.
The tablet contains two antiretriviral drugs, tenofovir and emtricitabine.
It does not prevent other sexually transmitted diseases or pregnancy.
PrEP may have the side effect of kidney dysfunction and minor gastro-intestinal problems.
9.8.7 The effects of HIV/AIDS
The effects include loss of fathers or mothers, economic loss, extra burden
on medical facilities, accepting HIV positive people in the
community.
To many patients with HIV/AIDS, loneliness is more fearsome than the illness
itself, and they say that while they could face death
straight on, few think they can bear being abandoned by their family and society.
However, people are showing concern and health workers should be ready
to give them medical and psychological care.
9.8.8 The ABC of protection
against HIV and the development of AIDS
A is for abstinence from engaging in sexual intercourse or delaying sexual
activity until marriage.
B is for being faithful to your sexual partner.
Both partners must be consistently faithful to each other
C is for correct and consistent condom use for all sexually active people
to control size of families and to protect against sexually
transmitted diseases.
9.9 Warts, genital warts
Warts, genital warts (Condyloma acuminata) Human Papilloma Virus (HPV)
The virus that causes the warts is called human papillomavirus (HPV).
See 5.3.2: Warts contact tracing, Human papilloma viruses (HPV)
Genital warts are caused by the Human Papilloma Virus, HPV.
Genital warts are very common in sexually active people with many sexual partners. but the warts may not be visible, e.g. warts on the cervix.
People who see or feel unusual lumps on the genitals should see a doctor.
Treat with paints, freezing or burning.
Repeat treatments are usually necessary.
Different strains of the wart virus affect different parts of the body.
Genital warts are different from warts seen on the hands and knees.
Genital warts are probably spread by sexual contact. but may not appear until months after infection.
Untreated genital warts are infectious and can be passed on to the sexual partners.
HPV is among the most common STDs in America and abroad, with an estimated 75% of all sexually active individuals infected by some strain of the disease.
HPV is best known, because of its connection in causing cervical cancer virus, but many strains also cause genital warts.
Symptoms: HPV is considered incurable, its symptoms can be treated, and many people resolve infections on their own.
Treatment: Recently the government approved a new vaccine to protect young women from the four most common strains of the virus.
Cryotherapy can freezing the abnormal cells with liquid nitrogen and conization removes the abnormal areas.
[conization: electrosurgical excision of cone of tissue from diseased uterine cervix]
LEEP or Loop Electrosurgical Excision Procedure removes lesions through electrical current.
5.3.2 Warts
Causative organism: Human papilloma viruses (HPV) usually types 6 &
11
Incubation period: 3 weeks to >12 months.
Most HPV infection is subclinical
Usual testing method: Clinical examination
Common symptoms: Anogenital warts
Likelihood of transmission per unprotected exposure High
Likelihood of long-term sexual partner being infected > 60%
Protective effect of condoms: Moderate
Transmission by oral sex: Rarely of clinical significance
Duration of potential infectivity: Months, probably years if HSV infection
is persistent
Important consequences: Psychosexual morbidity
Possibly enhanced HIV transmission
Direct benefit of detection and treatment of contacts: None, unless already
symptomatic
How far back to trace Contact tracing not recommended
Usual management of contacts: Counselling
Contact tracing priority: Low and not recommended
The majority of partners are probably already infected subclinically.
Notification: Not notifiable.
9.10 Zika virus
Zika virus Zika fever rash, fever, red or swollen eyes, pain in joints,
The Zika virus is on the move and new measures are needed to help to slow it down.
It is a distressing and disturbing infection that may be linked to thousands of babies being born with microcephaly.
It is spreading through the Americas.
Threats from the same virus family are increasing.
Currently, there is no effective treatment or vaccine against the Zika virus
The best way to protect yourself is to avoid being bitten by mosquitos.
The Brazilian Ministry of Health will distribute 500, 000 tests to perform Zika virus diagnostics.
As a result, public laboratories will expand 20 times to assist with this extra surveillance.
9.11 Virus diseases of plants
Viruses may cause yellow patches on leaves and later the plant dies, e.g. in taro and bananas.
These diseases cannot be cured, but if the virus is carried by insects they may be controlled.
The best way to deal with bacterial or virus diseases is to burn the infected plant or part of the plant.
Diseases are carried to plants in four ways:
1. Wind can carry diseases a short distance.
2. Disease can be carried in running water or in the splash of rain drops.
3. Infected plants can pass disease to healthy plants if the plants are touching.
4. Disease can be carried by insect pests that can then infect healthy plants.
Virus diseases include apple mosaic, clover stunt and cymbidium virus of orchids.
Yellow crinkle of papaya and big bud of tomatoes are caused by mycoplasma-like organisms (phytoplasmas).
9.12 ToBRFV, New tomato virus, 19/02/2020
Tobamoviruses include Tobacco Mosaic Virus (TMV) and Tomato Mosaic Virus (ToMV).
ToBRFV can overcome all known genetic resistance in tomato, including the Tm-22 gene.
It can cause severe fruit symptoms on otherwise resistant tomato varieties.
Pepper is another primary host for ToBRFV.
The L genes for resistance to TMV and PMMoV (Pepper mild mottle virus) in pepper currently seem to hold up to ToBRFV.
Peppers without the resistance gene(s) are highly susceptible to the virus.
Transfer of the virus from infected to healthy plants commonly occurs via mechanical means, e.g. touching and manipulation of infected plants.
ToBRFV is similar to other tobamoviruses in that the virus particles are long, symmetrical rods, so it cannot be distinguished by observation by electron microscopy.
Tomato F1 cultivars that are highly resistant (HR) to ToMV and TMV can be severely affected by this new virus. ToBRFV.
The known resistance genes do not protect against ToBRFV, and only preventative crop management and sanitation practices will produce a useful crop.
Some tomato varieties can develop a high virus level without physically expressing symptoms, so infected plants of these varieties can then become a source for spread of ToBRFV infection to healthy tomato plants or susceptible pepper plants.
Seed companies are working on identifying and introducing resistance to the virus in new varieties, but it could take several years, until new resistant varieties are introduced.
9.13 Tobamovirus
Tobamovirus is a genus in the virus family Virgaviridae.
The name "Tobamovirus" comes from the first virus discovered, (Tobacco mosaic virus).
Tobamovirus is a genus of plant viruses with a rigid helical rod containing linear single-stranded ribonucleic acid.
Tobacco mosaic virus is the type species and is also known as Tobacco mosaic virus group.
Classification
* Bell pepper mosaic virus (BPeMV), Brugmansia mild mottle virus, Cactus mild mottle virus (CMMoV),
* Clitoria yellow mottle virus, Cucumber fruit mottle mosaic virus, Cucumber green mottle mosaic virus (CGMMV)
* Cucumber mottle virus, Frangipani mosaic virus (FrMV), Hibiscus latent Fort Pierce virus (HLFPV)
* Hibiscus latent Singapore virus (HLSV), Kyuri green mottle mosaic virus, Maracuja mosaic virus (MarMV)
* Obuda pepper virus (ObPV), Odontoglossum ringspot virus (ORSV), Paprika mild mottle virus
* Passion fruit mosaic virus, Pepper mild mottle virus (PMMoV), Rattail cactus necrosis-associated virus (RCNaV)
* Rehmannia mosaic virus, Ribgrass mosaic virus (HRV), Sammons's Opuntia virus (SOV)
* Streptocarpus flower break virus, Sunn-hemp mosaic virus (SHMV), Tobacco latent virus
* Tobacco mild green mosaic virus, Tomato brown rugose fruit virus (ToBRFV), Tomato mosaic virus (ToMV)
* Tobacco mosaic virus (T2MV) - (Type species of genus Tobamovirus), Tomato mottle mosaic virus,
* Tropical soda apple mosaic virus, Turnip vein-clearing virus (TVCV), Ullucus mild mottle virus,
* Wasabi mottle virus (WMoV), Yellow tailflower mild mottle virus,
* Youcai mosaic virus (YoMV) aka oilseed rape mosaic virus (ORMV)
* Zucchini green mottle mosaic virus
9.14 Virus list
Plants
Bacteriophage (T type) (host E coli)
Broad bean wilt virus on legumes
Clover stunt virus on legumes
Cucumber mosaic virus
Cymbidium virus of orchids
Infection variegation of Camellia japonica
Iris mosaic virus
Leaf roll of potato virus
Lettuce big vein virus
Lettuce necrotic yellows virus
Potato mosaic virus, Potato Virus X
Rose mosaic
Tobacco mosaic virus
Tomato spotted wilt virus on tomato, capsicum, dahlia, chrysanthemum
Turnip mosaic virus
Woodiness of passion fruit virus