Life cycle of Aedes Aegypti mosquito

This is the life cycle of the Aedes aegypti mosquito. To prevent dengue fever, you must prevent the breeding of its carrier, the Aedes mosquitoes. Aedes mosquitoes are identified by the black and white stripes on their body. You can get rid of the Aedes mosquito by frequently checking and removing stagnant water in your home.

Therefore we must destroy the sources of the transmission of the virus the mosquito.
Firstly, we must prevent the mosquito from breeding as there will be more offspring to infect people. The mosquito lays the eggs in stagnant water, a 20cent coin height of water is enough for the mosquito to lay its egg and to grow into larva. Hence we can remove the stagnant water or we can put a layer of oil on the surface to kill the larva as there is no oxygen due to the oil.

Secondly, if you have been noticing every 2 weeks or 1 month there are people spraying insecticide to kill the mosquitoes present in the neighborhood. We can also protect ourselves by putting mosquito screen over our bed when we are sleeping.

Here are some interest facts about the aedes aegypti mosquito.

Fast facts about the mosquito
•Only the female aedes mosquito bites as it needs the protein in blood to develop its eggs.

•The mosquito becomes infective approximately 7 days after it has bitten a person carrying the virus. This is the extrinsic incubation period, during which time the virus replicates in the mosquito and reaches the salivary glands.

•Peak biting is at dawn and dusk.

•The average lifespan of an Aedes mosquito in Nature is 2 weeks

•The mosquito can lay eggs about 3 times in its lifetime, and about 100 eggs are produced each time.

•The eggs can lie dormant in dry conditions for up to about 9 months, after which they can hatch if exposed to favourable conditions, i.e. water and food

Finally here is a video to create awareness about the Dengue fever which is spread by the aedes aegypti mosquito. Now sit back and enjoy…
http://www.dengue.gov.sg/images/materials/aedes.wmv

By Amas Goh

How do you know if you have dengue fever?

Continuing from my previous post, how do the doctors find out if we have dengue fever?
The classic picture is high fever with no localising source of infection, a petechial rash with thrombocytopenia and relative leukopenia - low platelet and white blood cell count. Care has to be taken as diagnosis of DHF can mask end stage liver disease and vice versa.
The WHO definition of dengue haemorrhagic fever has been in use since 1975; all four criteria must be fulfilled:
1.Fever, bladder problem, constant headaches, severe dizziness and loss of appetite.

2.Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea)

3.Thrombocytopenia (<100,000 platelets per mm³ or estimated as less than 3 platelets per high power field)

4.Evidence of plasma leakage (hematocrit more than 20% higher than expected, or drop in haematocrit of 20% or more from baseline following IV fluid, pleural effusion, ascites, hypoproteinemia)

5.Encephalitic occurences.


Dengue shock syndrome is defined as dengue hemorrhagic fever plus:
•Weak rapid pulse,
•Narrow pulse pressure (less than 20 mm Hg)
•Cold, clammy skin and restlessness.

Serology and polymerase chain reaction (PCR) studies are available to confirm the diagnosis of dengue if clinically indicated.

Have you ever wondered what had caused the deadly type of dengue fever- dengue haemorrahgic fever?

(1)Virulent strain theory and Antibody enhancement Some strains are more virulent than others (DEN-2). All 4 strains are different but there are some similarities. With prior infection (eg Den-1), the antibodies are able to recognize DEN-2 (current infection). This had caused the body to over response. The immune cell produces too much chemicals, which causes the plasma in the blood to leak out due to the inflammation which leads to low blood pressure and lastly SHOCK!

(2)Due to Severe acute respiratory syndrome


Lastly, there is no drugs and workable vaccines to cure Dengue Fever yet and hence the best way is to prevent yourself from getting it, which will be explained in another post. Chill out for now =)

By Amas Goh

What is this mosquito doing here?

Beeeeeeezzzzing………… A black-white mosquito had just flown past me and I immediately killed it instantly without any remorse...
This mosquito is called the Aedes aegypti transmits the Dengue Fever. It is a disease caused by infection with a dengue virus. There are four types of this virus (Den 1 to 4 ) which can infect you. Den-2 is the most antigenic and genotypic distance from the others. The dengue virus causes (1) Dengue Fever which is not quite deadly
(2) Dengue Haemorraghic Fever/Dengue Shock Syndrome which is the deadly type

Ouch… I have been bitten by a mosquito, does it means that I have dengue fever? No you don’t, you must have the follow symptoms first.
•Fever, headache, retro-orbital pain
•Muscle pain, bone pain, vomiting and nausea
The classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the disease (the so-called biphasic pattern). Clinically, the platelet count will drop until the patient's temperature is normal.

Symptoms for Dengue Haemorrahgic Fever (DHF) also show higher fever, variable haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate.

Did you know that when DHF combined with a cirrhotic liver has been suspected in rapid development of Hepatocellular Carcinoma. Given the DEN virus is related to the Hepatitis C virus this is an avenue for further research as HCC is the leading Cancer cause of death outside of Europe and North America. Normally HCC does not normally occur in a cirrhotic liver for 10+ years after the cessation of the poisioning agent. DHF patients can develop HCC within one year of cessation of abuse.

By Amas Goh

SPOOKY! HIV

‘‘Fossil’’ HIV reveals virus history
A preserved specimen of lymph node nearly half a century old has revealed how rapidly the HIV virus has diversified, according to international research. A team of researchers from around the world has been trawling through decades-old tissue samples from African hospital archives in the hope of finding samples containing the HIV virus. They struck it lucky with a sample that was collected back in 1960, from a woman living in what is now the Democratic Republic of Congo. This is the second-oldest sample of the HIV virus ever found - the oldest is from 1959.The researchers found that the HIV viral sequences these two samples differ significantly in their genetic makeup. .
Using a technique called molecular clock analysis; they were able to plot the two viral sequences' evolutionary path back in time to determine when they diverged. They concluded the strains evolved from a common ancestor that emerged in Africa near the beginning of the twentieth century around 80 years before the disease appeared in western populations."HIV mutates so quickly that 40 to 50 years old is really akin to looking at fossil bone that's millions of years old," he says. Extracting the viral genetic material from the samples was no easy task. The samples had been preserved in formalin, which can cause considerable damage to DNA sequences

HIV article

Gels to protect women from HIV may help men more By Maggie Fox, Health and Science Editor
Mon Jul 7, 10:34 PM ET

WASHINGTON (Reuters) - Gels aimed at helping women protect themselves from the AIDS virus may end up helping men as much or more, researchers predicted on Monday. Computer models predict that if and when such gels or creams are perfected, they would reduce the risk that men could get the incurable virus from women.
But women who use such gels, or microbicides, could end up with fewer treatment options if they do become infected with HIV anyway, said Sally Blower of the University of California, Los Angeles, and David Wilson of the University of New South Wales in Sydney, Australia.
"Paradoxically, although microbicides will be used by women to protect themselves against infection, they could provide greater benefit to men," they wrote in the Proceedings of the National Academy of Sciences.
A microbicide is a gel or cream that could be applied vaginally or rectally to protect against sexual transmission of the human immunodeficiency virus that causes AIDS.
None are on the market now, although several are being tested. Two versions use HIV drugs such as tenofovir which is usually taken orally to suppress the virus.
Blower and Wilson wanted to see if women risked developing resistance to such drugs if they used a microbicide but got infected anyway. Their idea is that the drugs can be absorbed into the body through the vaginal wall and then, like any other drug, could cause the AIDS virus to mutate.
Blower said their mathematical models predicted this was indeed possible, especially under real-world circumstances when some people like sex workers might not use the products consistently.
"What we found out that was interesting or surprising or paradoxical, was that under some conditions males would actually benefit a lot more than females," Blower said in a telephone interview.
"You would actually prevent a lot more infections in men than in women. That was surprising."
For their models Blower and Wilson used data taken from ongoing trials of microbicides, along with what is known about how HIV develops resistance to existing drugs and how consistently people use drugs and condoms.
If an eventual microbicide was not 100 percent effective, and if women did not use it consistently, then a certain percentage of women would get HIV anyway. Some of these women would continue using the microbicide but not take cocktails of HIV drugs, and so would develop resistance.
Often, drug-resistant HIV is less likely to be transmitted from one person to another, Blower said. So male sex partners of such women might be protected from HIV.
An estimated 33 million people have HIV, mostly in Africa. More than 61 percent of Africans with HIV are women who were infected by their husbands or other male sexual partners.
Most of the 3 million people who get HIV every year globally are women.
Condoms prevent infection but many men refuse to use them. Experts say women, and some men, need a private way to protect themselves.
"At the moment, there is absolutely nothing that women can do to protect themselves from HIV -- condoms are not in women's control," Blower said.

Did you know that normal skin is more vulernable to HIV than unhealthy skin?

Normal skin vulnerable to HIV

CHICAGO - INSTEAD of infiltrating breaks in the skin, HIV appears to attack normal, healthy genital tissue in women, US researchers said on Tuesday in a study that offers new insight into how the Aids virus spreads.

They said researchers had assumed the human immunodeficiency virus, or HIV, sought out breaks in the skin, such as a herpes sore, in order to gain access to immune system cells deeper in the tissue.

Some had even thought the normal lining of the vaginal tract offered a barrier to invasion by the virus during sexual intercourse.

'Normal skin is vulnerable,' Dr Thomas Hope of Northwestern University's Feinberg School of Medicine said in a telephone interview.

'It was previously thought there had to be a break in it somehow,' said Dr Hope, who is presenting his findings at a meeting of the American Society for Cell Biology in San Francisco.

He said until now, scientists had little understanding of the details of how HIV is transmitted sexually in women.

Dr Hope and colleagues at Northwestern in Chicago and Tulane University in New Orleans developed a new method for seeing the virus at work. They studied newly removed vaginal tissue taken from hysterectomy surgeries, and introduced the virus which carried fluorescent, light-activated tracers.

They watched under a microscope as the virus penetrated the outer lining of the female genital tract, called the squamous epithelium. They also observed the same process in nonhuman primates.

In both cases, they found HIV was able to quickly move past the genital skin barrier to reach immune cells, which the virus targets.

Dr Hope said the study suggests the virus takes aim at places in the skin that had recently shed skin cells, in much the same way that skin on the body flakes off.

The finding casts doubt on the prior theory of the virus requiring a break in the skin or gaining access through a single layer of skin cells that line the cervical canal.

And it might explain why some prevention efforts have failed. Dr Hope said one clinical trial in Africa in which women used a diaphragm to block the cervix had no effect at reducing transmission of the virus. Nor have studies of drugs designed to prevent lesions in genital herpes proven effective.

Dr Hope said the findings emphasise the need for treatments such as a vaccine to prevent infection.

And it makes clear the need for the use of condoms, which are highly effective at preventing infection.

'People need to remember that they are vulnerable,' Dr Hope said. 'The sad part is if people just used a condom, we wouldn't have this problem.'

In the United States, HIV is mostly passed among men who have sex with men. Females account for 26 per cent of all new HIV cases in the United States, according to the US Centres for Disease Control and Prevention.

Globally, HIV is more commonly spread by heterosexual sex.

The virus has infected 33 million people globally and has killed 25 million. -- REUTERS

Source: http://www.straitstimes.com/Breaking...ry_315397.html
By Amas goh

Master HIV replication cycle in just 7 STEPS?

Hi all is me again! Today I have found something interesting and we can master the HIV virus life cycle in just 7 pictures!!



[click image to enlarge it]
http://www.sciam.com/article.cfm?id=hiv-life-cycle-basics
Click on the link to see how the 7 pictures combined into 1 flash animation whereby steps of the HIV replication cycle are explained with pictures and are very detailed.
By Amas Goh

HIV AGAIN!

HIV is a retrovirus is any of a group of viruses that contain two single-strand linear RNA molecules per virion, which means it carries its genetic blueprint in the form of ribonucleic acid (RNA) instead of deoxyribonucleic acid (DNA). Additionally, the enzyme reverse transcriptase is employed to copy its genome into the DNA of the host cell's chromosomes. Usually the cellular process involves transcription of DNA into RNA. Reverse transcriptase makes it possible for genetic material to become permanently incorporated into the DNA genome of an infected cell.HIV infection mostly occurs through sexual contact.It can also be transmitted via blood such as sharing of needles or blood transfusionStudies have shown that HIV is not transmitted through contact such as touching or sharing towels, bedding, utensils.It is important to acknowledge that it is not sex that transmits HIV, but certain bodily fluids: blood, semen, vaginal secretions and breast milk.High-risk behaviors that can result in HIV transmission are sharing needles for drugs, tattoos, body piercing, with an HIV-infected person and/or engaging in unprotected anal, vaginal or oral sex with a person who is HIV infected. The virus also can be transmitted from an HIV-infected mother to her child through pregnancy, birth or breastfeeding.People contracted with other sex diseases are more prone to be affected during sex with an infected partner because mucous membranes are porous and viruses and other pathogens are able to pass through, these areas are rich in immune cells. When a person already has a sexually transmitted disease, sex organs may be flooded with CD4+T cells, making it much easier for HIVto infect.Also it is not unusual for HIV-infected persons to experience symptoms years after the initial infection; some may be symptom free for over 10 years. However, during the asymptomatic period, the virus is actively multiplying and destroying cells in the immune system, weakening the body's ability to fight infection. The effect is most keenly observed in the decline of the immune system's key infection fighters in the blood, the CD4+T cells

AH AIDS!

I have notice a rising number of people getting HIV Or Aids. This troubles me alot... is it because we as human are indecent ? Or is it we have no sense of having safe Sex Or is it people are jus pure unlucky..Anything can happen to any of us reading this webpage here .Who knows what will happen the moment after u leave your home.... maybe u were run over by a lorry , sent to a nearby hospital for treatment but very unlucky, one of the blood packet contain HIV genome and tada.... your infected !.. so i personally felt that people should start to notice the importance of preventing getting the virus or seek treatment .
Actually MANY people does not know that actually u does not get aids immediately you have to get the HIV first before your immune system is down and other diseases infect you.
Aids is Acquired Immunodeficiency Syndrome (AIDS) is the final stage of HIV infection. An infection takes the "opportunity" provided by the weakened immune system to cause an illness that is usually controlled by a healthy immune system These infections are sometimes life-threatening and require medical intervention to prevent or treat serious illnesses. Persons living with advanced HIV infection suffer opportunistic infections of the lungs, brain, eyes and other organs. The 26 CDC-defined AIDS indicator illnesses are opportunistic infection.(http://www.hiv.com/)
To stop aids u have to start from HIV and to stop HIV! U have to….
Practicing safe sex and avoiding high-risk behaviors
using a latex condom
Symptoms of HIV
According to the Centres for Disease Control and Prevention, the following are symptoms that may be warning signs of HIV infections:
-Rapid weight loss
-Dry cough
-Recurring fever or profuse night sweats
-Profound and unexplained fatigue
-Swollen lymph glands in the armpits, groin or neck
-Diarrhoea that lasts for more than a week
-White spots or unusual blemishes on the tongue, in the mouth or in the throat
-Pneumonia
-Red, brown, pink or purplish blotches on or under the skin or inside the mouth, nose or eyelids
-Memory loss, depression and other neurological disorders

Orthomyxoviridae

Orthomyxoviridae
• Genus Influenzavirus A
• Genus Influenzavirus B
• Genus Influenzavirus C
• Genus "Thogoto-like Viruses"
• Infects vertebrates.

• Virions contain 7 segments of to 8 segments of linear negative-sense single stranded RNA.

• Genome length - 12000-15000 nt. Longest 2300-2500 nt, second longest 2300-2500 nt, third 2200-2300 nt, fourth 1700-1800 nt, fifth 1500-1600 nt, sixth 1400-1500 nt, seventh 1000-1100 nt, eighth 800-900 nt.

• Has terminal repeated sequences; repeated at both ends. Terminal repeats at the 5'-end 12-13 nucleotides long, at the 3'-end 9-11 nucleotides long. Encapsidated genomic nucleic acid. Virus may contain defective interfering copies of nucleic acid.

• Virus can exist in different forms during cycle

• Envelop can be in spherical (50-120 nm diameter), or filamentous (20 nm diameter and 200-300(-3000) nm length).

• 500 spikes (projecting 10-14 nm from the surface), in which some dispersed evenly over virus (haemagglutininesterase (HEF)) while some are in clusters (haemagglutinin (HA) major glycoprotein is intervened unevenly by clusters of neuraminidase (NA), ratio of HA to NA about 4-5:1).
• Nucleocapsid(s) enclosed within lipoprotein membrane; nucleoproteins of different size classes with loop at each end. Nucleocapsids filamentous; with no clear modal length (of different size classes); 50-130 nm long; 9-15 nm in diameter. Symmetry helical.

Influenza A
Further classified, based on viral surface antigens hemagglutinin (HA or H), 16 subtypes and neuraminidase (NA or N), 9 subtypes.
Strains identified by standard nomenclature specifying virus type, geographical location where first isolated, sequential number of isolation, year of isolation, and HA and NA subtype. E.g. A/Moscow/10/99 (H3N2), B/Hong Kong/330/2001
Type A most infectious and most severe human-infecting virus among three influenza types. Some serotypes confirmed in humans are H1N1 (Spanish Flu), H2N2 (Asian Flu), H3N2 (Hong Kong Flu), and H5N1 (Avian Flu)
Influenza B
Less common than influenza A.
Known to only infect humans and seals
Mutates 2-3 times lower than type A and less genetically assorted (only 1 influenza B serotype). As a result, a degree of immunity to influenza B is usually acquired at an early age.
Pandemics of influenza B do not occur because influenza B does not mutate to extent that lasts immunity, which ensures reduced rate of antigenic change and limited host range.
Influenza C
Infects humans and pigs, and can cause severe illness and local epidemics.
Less common than other types and usually seems to cause less severe diseases in children.
Thogotovirus
Can replicate in both tick and vertebrate cells
Usually transmitted by ticks.
Can spread from infected to uninfected ticks when co-feeding on uninfected guinea-pigs, even though guinea-pigs are asymptomatic to virus.
THOV (6 RNA segments) isolated from ticks in Africa and southern Europe and known to infect humans in natural settings.
DHOV (7 RNA segments) isolated from ticks in India, eastern Russia, Egypt, and southern Portugal and is able to infect humans, causing a febrile illness and encephalitis.

Acknowledgements
http://en.wikipedia.org/wiki/Orthomyxoviridae
http://en.wikipedia.org/wiki/Thogotovirus
http://www.virology.net/Big_Virology/BVRNAortho.html

Picornaviridae & Orthomyxoviridae

Cold – Picornaviridae
Influenza – Orthomyxoviridae

Though picornaviruses are named for their small (“pico” + “RNA” = picorna) size, they include a large and diverse array of viruses – over 200 serotypes. These viruses can be traced all the way back to Ancient Egyptian records of polio epidemics, but are still around and cause a menagerie of diseases today, from polio to hepatitis A to the “common cold.”

· Picornaviruses contain positive sense, single-stranded RNA that is approximately 7-8 kilobases long.
· The genome is monopartite and polyadenylated at the 3’ end, but has a VPg protein at the 5’ end in place of a cap.
· The viral RNA is infectious and replication takes place in the cytoplasm.
· The virus has an IRES (Internal Ribosomal Entry Site) which distinguishes it from many other RNA viruses.
· The virus is naked with an icosahedral capsid.
· The capsid is one of the smallest of all viruses with a diameter of only 27-30nm.

Picture of picornaviridae

Control
- wash hands
- do not sneeze anywhere other than a tissue or handkerchief
- avoid people with cold
- stay home and rest well if you’re down with flu or cold

Do you know?

It is not possible to be immune to cold or flu as they have many different serotypes circulating simultaneously... And a large amount of virus is present in nasal discharge.

Avian Flu H5N1..what is it about?

Today I was surfing on youtube.com and I have found 2 very interesting videos about H5N1 virus also known as bird flu. The video talks from the most basic general knowledge needed to know what is the virus about and it also further explains the mechanism on how the virus can be spread from animal to human for example from a bird to a pig to a human. Therefore we must prepare for the next pandemic/epidemic that might occur in the future…





By Amas goh

Important for people who have sex with multiple partners!!

To the readers, if you have unsafe sex with multiple partners and shares intravenous drugs, you are at HIGH RISK for Hepatitis B. The disease spread through contact with infected blood or other body fluids of people who have hepatitis B. People who use intravenous drugs can get hepatitis B when they share needles with someone who has the virus. Pregnant women who are infected with hepatitis B can also pass the virus on to their babies. Hence, think twice before you act.

If you indulge in such activities you should see if you have these symptoms which arises through Acute Hepatitis B
Symptoms:
• nausea
• vomiting
• loss of appetite
• abdominal pain
• jaundice (the skin turns yellow)
• weakness
• fatigue
• brown urine (may look like tea)
Symptoms of hepatitis B can range from mild to severe. If you have a mild case of hepatitis, you may not even realize that you have it. It may not cause symptoms or may only cause symptoms similar to the stomach flu.

After reading what I have said about chronic and acute Hepatitis B, do you really understand what the differences between acute and chronic hepatitis B are?

When you are having symptoms for the first time, this is called acute hepatitis. Acute hepatitis lasts 6 weeks or less. Most people recover from the infection and have no long-lasting problems.

Hepatitis B can become an illness that lasts a long time. This is called chronic hepatitis B. It lasts six months or longer. Chronic hepatitis occurs when the liver has been damaged from the acute illness and can't recover. Chronic hepatitis develops in 10% to 20% of people who have hepatitis B.

People with chronic hepatitis B may not have any symptoms at all. In some people, chronic hepatitis can lead to cirrhosis of the liver. Cirrhosis occurs when the liver cells die and are replaced by scar tissue and fat. The damaged areas of the liver stop working and can't cleanse the body of wastes. Cirrhosis can lead to liver failure and even liver cancer.

If you have hepatitis B, you are also susceptible to hepatitis D (also called "Delta agent). Hepatitis D can only develop in people who already have hepatitis B. It can make your symptoms of hepatitis B or liver disease worse. It is spread through contact with infected blood or other body fluids of people who have hepatitis D.
The time between the acute illness and signs of chronic hepatitis B varies. It may take a short time, or it may be years after the acute infection before chronic hepatitis B develops.
By Amas goh

How to diagnose, treat and prevent contracting Hepatitis B.

Hey it is me again! Today I will be talking on how to diagnose, treat and prevent yourself from contracting Hepatitis B.

The tests for detection of hepatitis B virus infection involve blood tests that detect either viral antigens or antibodies produced by the host. The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. The infectious virion contains an inner "core particle" enclosing viral genome known as hepatitis B core antigen, or HBcAg. During this stage the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM) may be the only serological evidence of disease.

After HbsAg appear, another antigen Hepatitis B e antigen (HBeAg) will appear. During the infection, the HBeAg may be cleared, and antibodies to the 'e' antigen (anti-HBe) will arise immediately afterwards. After the infection HBsAg will become undetectable and will be followed by IgG antibodies to the hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc IgG). A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously.

Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers. Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase levels and inflammation of the liver, as revealed by biopsy (cutting a small piece of liver for testing)


This picture shows what happens during and after the infection period

In adults, Acute hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously, if not antiviral drugs can be given. For chronic infection, Interferon alfa-2b and other antiviral medicines will be given. Treatment may take a year or more, depending on the severity of the infection and the response to treatment.

After knowing all theses, we need to protect ourselves and our love one. So how do we do it?

The best way to prevent hepatitis B is to have protected sex (use a condom) and to avoid sharing needles. A vaccine is available to prevent hepatitis B. It is now routinely given in the first year of life to all newborn infants. It is safe and requires 3 shots over a 6-month period. This vaccine should be given to people who are at high risk for this illness, such as health care workers, all children, drug users, people who get tattoos or body piercing, and those with multiple sex partners.

Finally, remember the golden rules, play with fire and you will be burned. So think twice before you have unsafe sex!!

By Amas Goh

How to do we get hepatitis A?

Fatigue, Fever, Nausea, Diarrhea, Appetite loss, Depression, Jaundice
Sharp pains in the right-upper quadrant of the abdomen, Weight loss, Itching

Although the virus is excreted in the feces towards the end of the incubation period, specific diagnosis is made by the detection of Hepatitis A virus specific IgM antibodies in the blood. IgM antibody is only present in the blood following an acute hepatitis A infection. It is detectable from one to two weeks after the initial infection and persists for up to 14 weeks. The presence of IgG antibody in the blood means that the acute stage of the illness is past and the person is immune to further infection. IgG antibody to HAV is also found in the blood following vaccination and tests for immunity to the virus are based on the detection of this antibody.
[Click to enlarge image]
During the acute stage of the infection, the liver enzyme alanine transferase (ALT) is present in the blood at levels much higher than is normal. The enzyme comes from the liver cells that have been damaged by the virus.

Hepatitis A virus is present in the blood, (viremia), and feces of infected people up to two weeks before clinical illness develops.

There is no specific treatment for hepatitis A. Sufferers are advised to rest, avoid fatty foods and alcohol (these may be poorly tolerated for some additional months during the recovery phase and cause minor relapses), eat a well-balanced diet, and stay hydrated. Approximately 15% of people diagnosed with hepatitis A may experience one or more symptomatic relapse(s) for up to 24 months after contracting this disease.

The United States Centers for Disease Control and Prevention (CDC) in 1991 reported a low mortality rate for hepatitis A of 4 deaths per 1000 cases for the general population but a higher rate of 17.5 per 1000, in those aged 50 and over. Death usually occurs when the patient contracts Hepatitis A while already suffering from another form of Hepatitis, such as Hepatitis B or Hepatitis C or AIDS.

Young children who are infected with hepatitis A typically have a milder form of the disease, usually lasting from 1-3 weeks, whereas adults tend to experience a much more severe form of the disease.

By Amas goh

Hepatitis A..What is that?

Did you know that the most widespread hepatitis A outbreak in the United States afflicted at least 640 people (killing four) in north-eastern Ohio and south-western Pennsylvania in late 2003. The outbreak was blamed on tainted green onions at a restaurant in Monaca, Pennsylvania.In 1988, 300,000 people in Shanghai, China were infected with HAV after eating clams from a contaminated river… So, what is Hepatitis A?


The Hepatitis virus (HAV) is a Picornavirus; it is non-enveloped and contains a single-stranded RNA packaged in a protein shell.

Hepatitis A is an acute infectious disease of the liver caused by Hepatitis A virus, which is most commonly transmitted by the fecal-oral route via contaminated food or drinking water. The time between infection and the appearance of the symptoms, is between two and six weeks and the average incubation period is 28 days.

Hepatitis A does not have a chronic stage and does not cause permanent liver damage. Following infection, the immune system makes antibodies against the hepatitis A virus that confer immunity against future infection. The disease can be prevented by good hygiene, sanitation and vaccination. The vaccine protects against the virus in more than 95% of cases for 10 years. It contain inactivated Hepatitis A virus providing active immunity against a future infection. The vaccine was first phased in 1996 for children in high-risk areas, and in 1999 it was spread to areas with elevating levels of infection.

The vaccine is given in two doses in the muscle of the upper arm. The first dose provides protection two to four weeks after initial vaccination; the second booster dose, given six to twelve months later, provides protection for up to twenty years.

When HAV is ingested, it enters the bloodstream through the epithelium of the oropharynx or intestine. The blood carries the virus to its target, the liver, where it lives and multiplies within hepatocytes and Kupffer cells. There is no apparent virus-mediated cytotoxicity, and liver pathology is likely immune-mediated. Virions are secreted into the bile and released in stool. HAV is excreted in large quantities approimately 11 days prior to appearance of symptoms or anti-HAV IgM antibodies in the blood. The incubation period is 15-50 days, and mortality is less than 0.5%.


The virus spreads by the fecal-oral route and infections often occur in conditions of poor sanitation and overcrowding. Hepatitis A can be transmitted by the parenteral route but very rarely by blood and blood products. Food-borne outbreaks are not uncommon, and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection. Approximately 40% of all acute viral hepatitis is caused by HAV. Infected individuals are infectious prior to onset of symptoms, roughly 10 days following infection.



Early symptoms of hepatitis A infection can be mistaken for influenza, but some sufferers, especially children, exhibit no symptoms at all. Symptoms typically appear 2 to 6 weeks, after the initial infection.

By Amas Goh

Hepatitis B- What is it about?

Did you know that Hepatitis B virus infects the liver of in humans, and causes an inflammation called hepatitis. It is a DNA virus cause viral hepatitis and has caused epidemics in parts of Asia and Africa. Chronic hepatitis B is a long-term infection of the liver that can sometimes develop after a bout of acute, or short term, hepatitis B.



Look at this cute virus, it is a member of the Hepadnavirus family. The virion consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity. The outer envelope contains embedded proteins which are involved in viral binding of, and entry into, susceptible cells.

Did you know that Hepatitis B virus is one of the smallest enveloped animal viruses with a virion diameter of 42nm? The surface antigen (HBsAg) is composed of the lipid and protein that forms part of the surface of the virion and is produced in excess during the life cycle of the virus. The genome of HBV is made of circular DNA, but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral DNA polymerase.

I found this video that will give a more detailed explanation on the Hepatitis B virus.



By amas goh

Herpesviridae

Any one knows that Herpesviridae are a large virus family that affect animal and human?
Herpesviruses all share a common structure—all herpesviruses are composed of relatively large double-stranded, linear DNA genomes encoding 100-200 genes encased within an icosahedral protein cage called the capsid which is itself wrapped in a lipid bilayer membrane called the envelope. Herpesvirus is unique because after primary infection virus normally remain latent , reactivation occur when (stress,expose to sunlight during menstrual period)
Virus hide in the nerves tissue. Causes viralencephalitis or if passed from mother
birth, may cause brain damage in the child.
Herpesvirus genome has a concentric virion which contain
-Inner core
-Icosahedral capsid
-Amorphous tegument
-Envelope (glycoprotein)

Pathogenesis

Herpes simplex viruses

-HSV1 (cold sores) –oral cavity

-HSV2 (genital herpes) -genital

Varicella Zoster virus
-Varicella (chicken pox) –respiratory tract, pharynx

- Herpes zoster (shingles)

-Cytomegalovirus –? Virus found in saliva, urine, semen,
cervial secretion, breast milk

-EBV –nasopharynx, salivary gland
Clinical Features

Cold sores -blisters around the mouth -1 week

-Also affect eyes, gum.

-Genital herpes -blisters, burning sensation, discharge -1 -3 weeks

-Fever

-Lesion all over body

-Scratched lesion lead to secondary infection!

-Scarring

-Dangerous in pregnant women!

-May affect nervous system

Hierarchical classification of virus



This classification of virus was created by Lwoff, R. W. Horne, and P. Tournier in 1962.
It consists of phylum - class - order - family - subfamily - genus - species - strain/type, based on the shared properties of virus

4 main properties are used:
1. Nature of the nucleic acid: RNA or DNA
2. Symmetry of the capsid
3. Presence or absence of an envelope
4. Dimensions of the virion and capsid

Virus families are ordered with genomics, the explanation of relationships through evolution by researching on nucleic acid and protein sequence. All families have suffix -viridae e.g. Caliciviridae, Picornaviridae, Reoviridae, while genera have suffix –virus e.g. in Picornaviridae family there are 5 genera: enterovirus, cardiovirus, rhinovirus, apthovirus and hepatovirus.

Acknowledgement: http://www.nlv.ch/Virologytutorials/Classification.htm

Baltimore classification

• I: dsDNA viruses (e.g. Adenoviruses, Herpesviruses, Poxviruses)
• II: ssDNA viruses (+)sense DNA (e.g. Parvoviruses)
• III: dsRNA viruses (e.g. Reoviruses)
• IV: (+)ssRNA viruses (+)sense RNA (e.g. Picornaviruses, Togaviruses)
• V: (-)ssRNA viruses (-)sense RNA (e.g. Orthomyxoviruses, Rhabdoviruses)
• VI: ssRNA-RT viruses (+)sense RNA with DNA intermediate in life-cycle (e.g. Retroviruses)
• VII: dsDNA-RT viruses (e.g. Hepadnaviruses)

Acknowledgement
http://en.wikipedia.org/wiki/Baltimore_classification

Different between virus and bacteria!

The Difference Between Viruses and Bacteria
Viruses are the smallest and simplest known life form. They are 10 to 100 times smaller than bacteria.
The biggest difference between viruses and bacteria is that viruses must have a living host - like a plant, or animal - to multiply, while most bacteria can grow on non-living surfaces.
Unlike bacteria, which attack the body like soldiers mounting a pitched battle, viruses are guerilla fighters. They don't attack so much as infiltrate. They literally invade human cells and turn the cell's genetic material from its normal function to producing the virus itself.
Bacteria carry all the machinery needed for their growth and multiplication, while viruses carry mainly information - for example, DNA or RNA, packaged in a protein and/or membranous coat. Viruses harness the host cell's machinery to reproduce. In a sense, viruses are not truly "living," but are essentially information (DNA or RNA) that float around until they encounter a suitable living host.
References: Food and Drug Administration May 2007
http://www.cfsan.fda.gov/

Virus structure!

Virus
A virus is a sub cellular organism with a parasitic intracellular life cycle. It contains either RNA or DNA but not both. A virus is a non-living thing since it does not meet the requirements of a living thing. But once it has a host, it starts to infect the host. A virus is made up of a virion which contains nucleic acid genome surrounded by protein. The basic objective of a virion is to transfer the viral genome to a cell where it starts to replicate. This requires 2 things which are structures to contain and protect nucleic acid genome and specific receptors on the virion surface which allows virus to enter the target cell.

Classification of virus

Virus Structure - Capsid
The capsid is the protein structure surrounding the viral genome which is assembled around the nucleic acid. The whole part is called nucleocapsid. The use of small protein subunits reduces amount of genetic code capacity that has to be dedicated to produce capsid proteins which are crucial as big viral genomes are very small by cellular standards. Protein components naturally align in the energetically favourable state thus certain structure is preferred. These structures have mostly icosahedral or helical symmetry.

Icosahedral Helical

Envelope
The envelope is derived from membranes of the host cell. Envelopment is roughly a passive process of picking up membrane from the cell. Before envelopment takes places, specific changes occur to the membrane. Changes to membrane fluidity is resulting from preferential incorporation of specific lipids. The most apparent change is presence of protein spikes or fringe when virion is viewed by electron microscope. The viral proteins have to be present in order to platform specific virus functions like binding to host cell.

Viral Genome Size
A large viral genome is still small by cellular standards means that virus can produce many proteins allowing a complex structure whereas viruses with small genome are restricted. Therefore bigger viral genome means that the complexity of the structure is more than those with small viral genome.

Viral genome types
• Double stranded(ds) DNA – These are often among largest of viral genomes
• Single stranded (ss) DNA – These are usually small genomes
• Ds RNA- Compared to all RNA genomes these are smaller than most DNA genome
• Ss RNA - Can be subdivided into (+) & (-) sense. Positive sense can function as mRNA and those that are complementary to mRNA are negative sense.

Viruses with RNA genomes use DNA intermediate stage to produce the RNA genome.
Viruses with DNA genomes use RNA intermediate stage to produce DNA genome

Virus cycle
Attachment
Entry
Uncoating
replication and expression
Assembly
Exit

Replication of Virus
A virion must protect the viral genetic material and it has to be capable of delivering it into host cell. The surface of any virus must have receptor/effectors to bind to the host cell. Binding is mediated on one side by specific viral proteins and the other side by cellular structures. The progeny virus genomes assemble into new viruses and are used to make more viruses.

T4 Phage?

Pictures of T4 Bacteriophage
Looks like an alien landing pod.
Bacteriophage attaches to surface of bacteria Escherichia coli (E. coli).
Once attached, it injects DNA into bacterium, which uses bacterium to generate more DNA to produce more of such bacteriophage. After cycle is complete, bacterium bursts and dies, releasing newly produced bacteriophages to continue infecting other bacteria.
Bacteriophages have been used as an antibiotic in the former Soviet Union and Eastern Europe. They are seen as a possible therapy against multi drug resistant strains of many bacteria.
T4 bacteriophage undergoes a lytic lifecycle. It takes about 30 minutes (at 37 °C) and consists of:
Adsorption and penetration (immediate)
Arrest of host gene expression (immediate)
Enzyme synthesis (starts after 5 mins)
DNA replication (starts after 10 mins)
Formation of new virus particles (starts after 12 mins)
Courtesy of: http://www.cellsalive.com/phage.htm, http://en.wikipedia.org/wiki/T4_phage

What is a virus?

Virus
What Is a Virus?
A virus is an extremely tiny infectious agent that is only able to live inside a *cell.
Viruses can be rod-shaped, sphere-shaped, or multisided. Some viruses look like tadpoles.
Basically, viruses are composed of just two parts. The outer part is a protective shell made of *protein. This shell is often surrounded by another protective layer or envelope, made of protein or lipids (fats). The inner part is made of genetic material, either *RNA or *DNA.
A virus does not have any other structures (called organelles) that living cells have, like a nucleus or mitochondria. These organelles are the tiny organs that maintain a cell's metabolism (life processes). A virus has no metabolism at all.
http://www.acnepain.com/virus.html

Welcome to the Viridae Portal

We are a group of students from NYP Molecular Biotecnology MB0803
This blog is designed for our Microbiology B blog assignment, it is also a one stop portal for the news information from the world of viruses.

This blog is maintained by Amas Goh Chun Kiat, Wilson Chew Hong Wen, Phua Yao xing , N. Mohan , Low Soon Huat. This is our first entry and hope that you will carry on supporting this blog thanks =) Cheer!