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Archive for September 1st, 2007

Viruses’ beginning innocuous

September 1, 2007

NEW YORK — What began as a ninth-grade prank, a way to trick already-suspicious friends who had fallen for his earlier practical jokes, has earned Rich Skrenta notoriety as the first person ever to let loose a personal computer virus.

Although over the next 25 years, Skrenta started the online news business Topix, helped launch a collaborative Web directory now owned by Time Warner Inc.’s Netscape and wrote countless other computer programs, he is still remembered most for unleashing the “Elk Cloner” virus on the world.

“It was some dumb little practical joke,” Skrenta, now 40, said in an interview. “I guess if you had to pick between being known for this and not being known for anything, I’d rather be known for this. But it’s an odd placeholder for (all that) I’ve done.”

“Elk Cloner” — self-replicating like all other viruses — bears little resemblance to the malicious programs of today. Yet in retrospect, it was a harbinger of all the security headaches that would only grow as more people got computers — and connected them with one another over the Internet.

Skrenta’s friends were already distrusting him because, in swapping computer games and other software as part of piracy circles common at the time, Skrenta often altered the floppy disks he gave out to launch taunting on-screen messages. Many friends simply started refusing disks from him.

So during a winter break from the Mt. Lebanon Senior High School near Pittsburgh, Skrenta hacked away on his Apple II computer — the dominant personal computer then — and figured out how to get the code to launch those messages onto disks automatically.

He developed what is now known as a “boot sector” virus. When it boots, or starts up, an infected disk places a copy of the virus in the computer’s memory. Whenever someone inserts a clean disk into the machine and types the command “catalog” for a list of files, a copy gets written onto that disk as well. The newly infected disk is passed on to other people, other machines and other locations.

The prank, though annoying to victims, is relatively harmless compared with the viruses of today. Every 50th time someone booted an infected disk, a poem he wrote would appear, saying in part, “It will get on all your disks; it will infiltrate your chips.”

Skrenta started circulating the virus in early 1982 among friends at his school and at a local computer club. Years later, he would continue to hear stories of other victims, including a sailor during the first Gulf War nearly a decade later. (Why that sailor was still using an Apple II, Skrenta does not know.)

These days, there are hundreds of thousands of viruses — perhaps more than a million depending on how one counts slight variations.

The first virus to hit computers running Microsoft Corp.’s operating system came in 1986, when two brothers in Pakistan wrote a boot sector program now dubbed “Brain” — purportedly to punish people who spread pirated software. Although the virus didn’t cause serious damage, it displayed the phone number of the brothers’ computer shop for repairs.

With the growth of the Internet came a new way to spread viruses: e-mail.

“Melissa” (1999), “Love Bug” (2000) and “SoBig” (2003) were among a slew of fast-moving threats that snarled millions of computers worldwide by tricking people into clicking on e-mail attachments and launching a program that automatically sent copies to other victims.

Although some of the early viruses overwhelmed networks, later ones corrupted documents or had other destructive properties.

Compared with the early threats, “the underlying technology is very similar (but) the things viruses can do once they get hold of the computer has changed dramatically,” said Richard Ford, a computer science professor at the Florida Institute of Technology.

Later viruses spread through instant-messaging and file-sharing software, while others circulated faster than ever by exploiting flaws in Windows networking functions.

More recently, viruses have been created to steal personal data such as passwords or to create relay stations for making junk e- mail more difficult to trace.

Suddenly, though, viruses weren’t spreading as quickly. Virus writers now motivated by profit rather than notoriety are trying to stay low-key, lest their creations get detected and removed, along with their mechanism for income.

Many of the recent malicious programs technically aren’t even viruses, because they don’t self-replicate, but users can easily get infected by visiting a rogue Web site that takes advantage of any number of security vulnerabilities in computer software.

Although worldwide outbreaks aren’t as common these days, “believe it or not there’s exponentially more malware today than there ever was,” said Dave Marcus, a research manager for McAfee Inc.’s Avert Labs. “We find 150 to 175 new pieces of malware every single day. Five years ago, it would have been maybe 100 new pieces a week.”

Symantec Corp. formed the same year Skrenta unleashed “Elk Cloner,” but it dabbled in non-security software before releasing an anti-virus product for Apple’s Macintosh in 1989. Today, security- related hardware, software and services represent a $38 billion industry worldwide, a figure IDC projects will reach $67 billion in 2010.

Information provided by: Findarticles.com

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We recently identified 2 Mokola viruses from domestic mammals (a dog and a cat) in South Africa, These cases occurred 8 years after the last reported case of infection with this virus, Our findings emphasize the endemicity of rabies-related lyssaviruses in South Africa and the need to better understand the epidemiology of Mokola viruses.

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Mokola virus (MOKV) is classified as genotype (gt) 3 of the genus Lyssavirus in the family Rhabdoviridae (order Mononegavirales). Apart from MOKV, the genus Lyssavirus consists of 6 gts: classic rabies virus (gt1), Lagos bat virus (gt2), Duvenhage virus (gt4), European bat lyssavirus type 1 (gt5) and type 2 (gt6), and Australian bat lyssavirus (gt7). Some novel lyssaviruses identified in bat species in the former Soviet Union are considered putative gts within this genus (1).

Although gt1 viruses have a global distribution, gt5 and gt6 viruses are restricted to Europe and gt7 viruses are limited to Australia. Natural infections with gt2, gt3, and gt4 viruses have been found only in Africa. With the exception of MOKV, all lyssavirus gts and putative gts have been isolated exclusively or most frequently from chiropteran species. MOKV has never been isolated from these species, but only from terrestrial mammals. The first MOKV was isolated from shrews (Crocidura sp.) in Nigeria in 1968. Since then, [greater than or equal to] 20 isolates of this lyssavirus have been found throughout Africa (Cameroon, Central African Republic, Ethiopia, South Africa, and Zimbabwe) (2-12) (Table 1).

We report the identification and characterization of 2 cases of infection with MOKV in South Africa. The first was in a domestic dog and is, to our knowledge, the first such case in South Africa. The second was in a domestic cat, the host species in which all previous isolates were found. The cat MOKV isolate belonged to 1 of 2 previously identified South African MOKV phylogenetic lineages, but the dog MOKV isolate appeared to have a different lineage not previously encountered in South Africa or elsewhere in Africa.

The Study

In October 2004, a 3-month-old kitten (Felis domesticus) was adopted from the Society of the Prevention of Cruelty to Animals (East London, Eastern Cape Province, South Africa) and lived with its owner on a farm 23 km outside the city. It had been neutered and had been vaccinated at 10 months of age with an adjuvanted inactivated vaccine against rabies (Rabisin; Merial, Lyon, France), but no subsequent vaccinations were given. The cat spent most of the day indoors, but went out at night and returned in the morning. Unusual behavior was noticed in March 2006. It appeared dull and physically unbalanced and its pupils were dilated but it was not aggressive. The cat was humanely killed, and its brain was sent to the Onderstepoort Veterinary Institute for rabies testing.

On June 17, 2005, a 6-month-old puppy (Canis familiaris) was brought by its owner to a veterinarian in the rural town of Nkomazi (Mpumalanga Province, South Africa). The dog had a temperature of 39.8[degrees]C and no appetite. After symptoms were treated, the dog was discharged, but it was brought back 11 days later because it was paralyzed, dehydrated, and had a fixed stare. This animal had never been aggressive to other pets or humans. The dog was humanely killed, and its brain was sent to the Onderstepoort Veterinary Institute for rabies testing.

Direct immunofluorescent antibody test with an anti-rabies conjugate cross-reactive with African lyssaviruses showed numerous and strongly stained inclusion bodies in every field of impression smears of both brain samples. Isolation of virus was attempted by suckling mouse brain passage and cell culture (neuroblastoma cells; Diagnostic Hybrids, Athens, OH, USA); both methods were successful for the cat sample. However, neither method yielded an isolate from the dog sample, despite a lyssavirus-specific reaction in the original brain sample by direct immunofluorescent antibody test.

Subsequently, antigenic characterization was performed with a panel of 16 monoclonal antibodies to the nucleocapsid protein of rabies virus (Canadian Food Inspection Agency, Nepean, Ontario, Canada). Both samples showed reactivity patterns associated with MOKV (Table 2).

Final confirmation of MOKV in both case samples was obtained by reverse transcription–PCR, nucleotide sequencing, and phylogenetic analysis as described (12). Phylogenetic analysis (Figure) showed that the virus isolated from the cat sample (designated MOKV173/06) belonged to the same lineage of MOKV isolates that were recovered from cats in the same region of South Africa (12). However, the virus detected in the dog sample (designated MOKV404/05) appeared to represent a different South African MOKV lineage that was phylogenetically positioned between known South African and Zimbabwean lineages. This MOKV had nucleotide similarities of 88.1%-90.4% and 85.3%-88.5% with viruses from Zimbabwe and South Africa, respectively.

Information provided by: Findarticles.com

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AXA Assistance USA said Aug. 9 it is caring for more than 73 UK tourists who fell ill due to a stomach virus outbreak at the Bahia Principe Puerto Plata Resort. More …

Read the rest of this article with a Free Trial at HighBeam Research.

Information provided by: Findarticles.com

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Background & objectives: Information on hepatitis C virus (HCV) infection in pregnant women in India is scanty. This study was carried out to investigate the prevalence of HCV within an obstetric population in north India and to identify the various risk factors for the viral infection.

Methods: A total of 8130 pregnant women from antenatal clinic were subjected to anti-HCV testing by third generation ELISA. Anti-HCV positive seropositive women were further tested for HCVRNA, hepatitis B and HIV. The women were evaluated for the presence of following known risk factors for HCV infection.

Results: Eighty four (1.03%) pregnant females had HCV antibodies. Of these, 46 (54.8%) were positive for HCV-RNA, 4(4.8%) tested positive for HBsAg, while none tested positive for HIV. The mean age and parity of the anti-HCV antibody positive women was 24.36±3.6 yr and 0.9±0.8, while that of the anti-HCV antibody negative women was 24.13±3.6 yr and 0.8±0.8 respectively. Of the 84 anti-HCV positive women, 52 (61.9 %) did not have any identifiable risk factors. The risk factors variables did not have significant association with HCV positive status.

Interpretation & conclusion: Prevalence of hepatitis C in pregnant women was 1.03 per cent. None of the known risk factors was found to be significantly associated with the HCV infection. Hence case identification and consequent management pose a particular problem and routine screening is not a viable option in our resource- poor setting.

Key words Anti-HCV antibody - hepatitis C virus infection - pregnancy - prevalence - risk factors

Hepatitis C virus (HCV) is one of the major aetiological agents of parenterally acquired hepatitis. HCV infection is asymptomatic in a large proportion of cases (65-75%) and revealed only accidentally by abnormal liver function tests and /or anti-HCV positivity. The long-term morbidity and mortality is far greater than its counterpart hepatitis B in terms of chronic active hepatitis (70%), cirrhosis (20-30%), hepatocellular carcinoma and liver failure1. Anti-HCV screening of blood products introduced during the early 1990s has minimized this mode of HCV acquisition, leaving vertical transmission from infected mothers as the predominant mode of infection in children. Approximately 7-8 percent of hepatitis C virus-positive women transmit hepatitis C virus to their offsprings with a higher rate of transmission seen in women co-infected with HIV2.

The worldwide literature on HCV prevalence has increased considerably over the past decade, yet few surveys have been conducted on national level. Several studies of pregnant women in Europe reported relatively low anti-HCV prevalence when second or third generation ELISAs were used. In an antenatal survey from England, the prevalence of anti-HCV in antenatal clinic attenders in Greater London area and Northern and Yorkshire region was found to be 0.43 per cent (of 25938 women) and 0.21 per cent (of 16675 women) respectively3. The HCV prevalence of 0.38 and 0.20 per cent were seen in inner and outer districts of London respectively4. Another UK study of an antenatal population in the West Midlands found an overall HCV prevalence of 0.14 per cent5. In a national survey among 30,259 childbearing women throughout Scotland, the HCV seroprevalence was found to be 0.29-0.40 per cent6.

Little is known about hepatitis C virus infection in pregnant women in India. The seroprevalence of anti-HCV antibody in the healthy general population of India was found to be 1.5 per cent each in 234 voluntary blood donors and 65 pregnant women7. HCV infection was not detected in 250 randomly selected antenatal women in Shimla (Himachal Pradesh)8. In our preliminary study, 14 of 1900 (0.73%) pregnant females were tested anti-HCV seropositive9. There are no large scale studies on the estimates of the prevalence of HCV infection and risk behaviour of HCV infection in low risk Indian population. We tiierefore undertook this study to assess the prevalence of HCV infection within an obstetric population attending a tertiary care hospital in New Delhi, India and to determine whether various risk factors for HCV infection could be identified.

Material & Methods

The study recruited a cohort of consecutive 8130 healthy pregnant women at the antenatal clinic of Department of Obstetrics and Gynecology of Maulana Azad Medical College and Lok Nayak Hospital, New Delhi, India (May 2004 to August 2006). Assuming the average prevalence of HCV infection to be 0.2 per cent (based on data available from western countries) and with a precision of 0.04 (20% of true estimate) and at a probability level of 10 per cent, it was estimated that nearly 8000 pregnant women need to be screened. Seventeen women were excluded who declined to participate (15) or who had liver diseases (2). The characteristics of these 17 women were comparable to that of those included in the study and were not taken for analysis in this paper. The Institute Ethics Committee approved the study. All women attending the antenatal clinic, who gave their consent to participate, were evaluated by a questionnaire. It dealt with detailed demographic characteristics and factors that could put a woman at risk for acquiring hepatitis C. The women with previous liver disease were excluded. Anti-HCV antibodies were detected by commercially available third generation ELISA diagnostic kits (SP-NANBASE C-96 3.0, manufactured by General Biological Corp, Taiwan). The initially reactive samples were re-tested in duplicate and considered ELISA positive if at least two of three results were reactive. All anti-HCV antibody positive samples were tested for HCV-RNA by a reverse transcriptase polymerase chain reaction (RT-PCR). RNA was extracted by using the acid guanidinium-phenol-chloroform method as described by Chomczynski and Sacchi10. All HCV antibody positive women were further tested for HBsAg, HBcIgG, HBeAg (kits manufactured by General Biological Corp, Taiwan) and human immunodeficiency virus (HIV) by Microlisa-HIV Elisa Kit manufactured by J. Mitra & Co. Pvt. Ltd., New Delhi, India. Each of the HCV positive patients was invited to participate in an interview with the first author (AK) at a subsequent antenatal visit for counselling. Serological results were told to them and they were counseled for the need of further postpartum follow up with the hepatologist.

Information provided by: Findarticles.com

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