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