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Not all viruses harm people. The Food and Drug Administration has approved a mixture of viruses as a food additive to protect people. The additive can be used in processing plants for spraying onto ready-to-eat meat and poultry products to protect consumers from the potentially life-threatening bacterium Listeria monocytogenes (L. monocytogenes).

The viruses used in the additive are known as bacteriophages. Bacteriophage means "bacteria eater." A bacteriophage, also called a phage (pronounced fayj), is any virus that infects bacteria.

Consuming food contaminated with the bacterium L. monocytogenes can cause an infectious disease, listeriosis, which is rarely serious in healthy adults and children, but can be severe and even deadly in pregnant women, newborns, older people, and people with weakened immune systems. Pregnant women are about 20 times more likely than other healthy adults to get listeriosis, according to the Centers for Disease Control and Prevention (CDC). Listeriosis can cause miscarriage, stillbirth, premature delivery, or death of a newborn baby.

People with listeriosis have fever and muscle aches, and sometimes an upset stomach, nausea, and diarrhea. If the infection spreads to the nervous system, headache, stiff neck, confusion, loss of balance, or convulsions can occur.

The CDC estimates that about 2,500 people become seriously ill with listeriosis each year in the United States. Of these, about 500 die.

Cooking can kill L. monocytogenes, but many ready-to-eat foods, such as hot dogs, sausages, luncheon meats, cold cuts, and other deli-style meats and poultry, may become contaminated within the processing plant after cooking and before packaging. Unlike fresh meat and poultry, the ready-to-eat products can be consumed without reheating, so the L. monocytogenes survive and are ingested.

"L. monocytogenes can continue to thrive even in refrigerated conditions," says Capt. Andrew Zajac, a food safety expert and acting director of the Division of Petition Review within the FDA’s Center for Food Safety and Applied Nutrition (CFSAN). "If a food product contaminated with L. monocytogenes is bought by a consumer and brought home and refrigerated, the bacteria can continue to multiply."

How Bacteriophages Work

Bacteriophages are found in the environment. "We’re routinely exposed to bacteriophages," says Zajac. "They are found in soil and water, and they are part of the microbial population in the human gut and oral cavity."

Bacteriophages infect only bacteria, says Zajac. "They don’t infect plant or mammalian cells." Thousands of varieties of phages exist, and each one infects only one type or a few types of bacteria. The particular phages approved as a food additive are very specific to Listeria, says Zajac. "They’ll only thrive if Listeria are present."

The type of phage that was approved is lyric, which means that the phage destroys its host during its life cycle without integrating into the host genome. This type of phage works by attaching itself to a bacterium and injecting its genetic material into the cell. The phage takes over the metabolic machinery of the bacterium, forcing it to produce hundreds of new phages and causing the bacterial cell walls to break open. This process kills the bacterium and releases many new phages, which seek out other bacteria to invade and repeat the cycle.

"The process continues until all host bacteria have been destroyed," says Zajac. "Then the bacteriophages cease replicating. They need a host to multiply and will gradually become inactive when they lose the host."

Approval Process for Food Additives

To market a new food additive, a manufacturer must petition the FDA for its approval. The petition must provide convincing evidence that the proposed additive performs as it is intended and will not cause harmful effects when consumed.

If an additive is approved, the FDA issues a regulation that includes information on the types of foods in which the additive can be used and maximum amounts to be used. The regulation also provides the additive’s identity and specifications on purity, which will ensure that the additive used in food is the same substance that was evaluated and approved by the FDA.

Once a food additive is approved, any company can use the additive, says Zajac, as long as it meets the conditions in the regulation.

In response to a petition submitted by industry, the FDA published a regulation in August 2006 permitting the use of a Listeria-specific bacteriophage preparation on ready-to-eat meat and poultry products.

The preparation combines six different phages that have been shown to be effective against 170 different strains of L. monocytogenes. Multiple phages are used so that if the L. monocytogenes develop resistance to several phages, the remaining ones can still destroy the bacteria.

The FDA must approve any additive before it can be used in food. When an additive is to be used on meat or poultry products, as with this one, both the FDA and the U.S. Department of Agriculture (USDA) are involved in the approval. The FDA evaluates the safety of the ingredient for its intended use. At the same time, the USDA evaluates the ingredient’s suitability.

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To the Editor: The global prevalence of dengue fever (DF) has grown dramatically in recent decades; DF is now endemic to >100 countries (1). Dengue hemorrhagic fever (DHF), a potentially lethal complication of dengue virus infection, was first recognized in Asia in the 1950s and is now a leading cause of hospitalization and death among children (1). During the past decade, DHF epidemics have occurred in China, Sri Lanka, India, the Maldives, Bangladesh, and Pakistan (2-4).

In Pakistan, an outbreak of DHF was first reported in Karachi in 1994 (4). Through mid-2005, 15-20 patients with DF or DHF were admitted each year to the Aga Khan University Hospital (AKUH), a tertiary care referral center in Karachi. Many more cases, however, may have gone unrecognized. Ours is the first report of dengue virus serotype 3 in Pakistan.

From September through December 2005, at least 3 major hospitals in Karachi, including AKUH, had a sudden increase in the number of patients with signs consistent with the World Health Organization definition of DHF: high fever, rash, epistaxis, gum bleeding, liver dysfunction, and thrombocytopenia (platelets <100,000/[mm.sup.3]); most had evidence of capillary leakage in the form of raised hematocrit and pleural effusion with or without ascites (5). Because in Pakistan, Crimean-Congo hemorrhagic fever (CCHF) is an important differential diagnosis for hemorrhagic fever, most patients seen at AKUH received care in strict isolation and were empirically treated with ribavirin. At time of admission, blood samples were collected for serologic testing for dengue virus and reverse transcription (RT)-PCR testing for CCHF virus. The first 5 samples, collected during the initial 2 weeks of the outbreak, were also sent to the Special Pathogens Reference Unit, Centre for Emergency Preparedness and Response, Health Protection Agency, Salisbury, United Kingdom, for diagnostic confirmation. In the absence of a local surveillance and disease notification system, the number of patients with suspected DHF at different hospitals in Karachi could not be ascertained.

Of the 106 patients who had a clinical diagnosis compatible with DHF (5), 9 (8.5%) died and 97 (91.5%) recovered. Patients with possible DF (fever, mild thrombocytopenia with platelets >100,000/[mm.sup.3]) were not admitted and were treated as outpatients. Dengue virus infection was confirmed for 42 of the 106 patients. Serum samples from 39 patients contained anti-dengue virus immunoglobulin M (IgM) antibody (Chemicon, Temecula, CA, USA). Diagnosis for 6 of these patients was confirmed by using immunoblot tests (Dengue IgM Blot and Dengue IgG Blot, Genelabs Diagnostics, Singapore). Of the 9 patients who died, 6 had dengue IgM and IgG according to immunoblot testing, and 3 had dengue IgM according to ELISA. Diagnoses for 3 additional patients were confirmed by RT-PCR.

An RT-PCR assay specific for dengue viruses (6) was used to amplify the C/PrM/M region of the genome and produced PCR products of the expected size in 3 patient samples: 2 (K1 and 2) from Karachi and 1 (B) from Balochistan. The PCR products were sequenced, and data were subsequently placed in GenBank under accession numbers DQ469827 for D3418-05 (patient K1), DQ469828 for D3419-05 (patient K2), and DQ469826 for D3417-05 (patient B). These data were compared with those in databases by using the basic local alignment search tool for nucleotides (blastn), with default settings (7). For each sequence analyzed, the lowest Expect (E) value showed significant similarity with a dengue serotype 3 isolate from India in 2004 (DQ323042). A phylogenetic tree was constructed with a collection of dengue sequences (online Appendix Table, available from www.cdc.gov/ncidod/EID/13/1/182-appT.htm). Phylo-genetic relationships between sequences are depicted in the Figure. Sequences from the 2005 outbreak are most similar to those from Indian strains of dengue serotype 3, which were isolated in Delhi.

[FIGURE OMITTED]

An unexpected finding was the detection, at both AKUH and the UK Special Pathogens Reference Unit, of dengue-3 and CCHF virus RNA in the sample from patient B. CCHF is endemic to the rural Balochistan province of Pakistan, where DF has been documented (8). In the absence of information on the current dengue situation in Balochistan and given the increasing dengue activity in Karachi, a similar increase can be assumed for Balochistan. Possible introduction of dengue serotype 3 in a CCHF-endemic area resulted in dual infection in patient B, who essentially had clinical and laboratory features compatible with DHF. Patient B received ribavirin and recovered. Our results suggest that the 2005 outbreak of DHF in Karachi, Pakistan, was caused by strains of dengue virus serotype 3 related to those circulating in India (9).

Acknowledgments

We thank Aslam Khan, Maqsood Bhatti, and Roshan Hadwani for their contributions to this work.

References

(1.) World Health Organization. Dengue and dengue haemorrhagic fever. Fact sheet no. 117; Revised 2002 Apr [cited 2006 Oct 31]. Available from http://www.who.int/mediacentre/factsheets/fs117/en/

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Infectious mononucleosis (IM) also known as mono or glandular fever, is a clinical syndrome caused by Epstein-Barr virus (EBV), the fourth human herpes virus. EBV is a member of the herpes-virus family–a gamma herpes virus, in fact–and infects over 95% of the world’s population, mostly with no adverse effects. (1) The timing of initial infection is crucial in dictating the symptoms experienced by the host. IM is the typical illness experienced by adolescents newly infected with EB whereas, in contrast, infants nearly always have asymptomatic infection. Infections are lifelong and do not usually carry any risk of future disease. But some features of the acute infection have significant clinical importance. Under certain circumstances, most commonly immunosuppression, EBV infection has been implicated in several types of human malignancy–Burkitt’s lymphoma being perhaps the best recognized, but also nasopharyngeal carcinoma and others. The laboratory can play a crucial role in diagnosing and managing EBV infection.

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EBV was first detected by Epstein, Barr, and Achong in a Burkitt’s lymphoma cell line in 1964, (2) and holds the dubious honor of being the first human tumor virus described. Four years later, Henle reported an association between EBV and infectious mononucleosis, (3) an observation that was later confirmed in a study of students at Yale University. (4)

EBV shares the classic structural features of the other herpes viruses: it is enveloped, contains a nucleoid and capsid, and has a linear double-stranded DNA genome, which is contained within the nucleoid structure. EBV can enter into a latent phase of replication, during which the genome persists as a circular episome in the cell nucleus, with only minimal activity of select viral genes. These genes ensure that the episome is replicated and transmitted to daughter cells as if it were a normal host chromosome, as well as being involved in reactivation and tumorigenesis.

The cell types naturally infected with EBV are the B lymphocyte, responsible for antibody production, and epithelial cells. The typical portal of entry is the mouth, with initial replication occurring in the nasopharynx, and EBV is secreted in saliva from infected salivary glands (which is why IM is also sometimes called the kissing disease). (5) Systemic spread results in seeding of organs such as lymph nodes, spleen, and liver; and abnormal liver enzyme levels are a common finding. The mononucleosis is not, in fact, from stimulation of B cells by viral infection (although EBV will transform cell lines in vitro), but is from a large, effective, CD8 cytotoxic T-cell response against the EBV-infected circulating B cells. (6) Once latent infection is established in epithelial cells and B lymphocytes, they become immortalized with occasional reactivation of lytic viral replication. After the initial infection, EBV may be continually secreted in saliva for up to 18 months, but even once the infection is brought under immune control, a large percentage of healthy asymptomatic people infected with EBV will shed the virus in saliva at any one time.

Populations affected; syndromes mimicked

Most of the clinical effects of EBV infection are found in the adolescent and adult populations, even though worldwide most infections occur in infants. This is due to the fact that in the developed world, the epidemiology is very different from that in developing nations. Additionally, dietary difference and exposures to other infectious agents modify the effects of EBV considerably.

In the United States, approximately 50% of the population is infected by five years of age, (7) although exact numbers are difficult to come by as EBV is not a reportable infection. Ninety percent of adults are infected by 25 years of age (in contrast to developing countries where 90% of people are infected by two years of age). In lower socio-economic groups, EBV infection tends to occur at younger ages and with a consequently lower rate of IM. Studies in the 1970s showed a thirtyfold higher risk of IM in the Caucasian population vs. African-Americans, but this was due to social differences and not any real racial predilection. (8) Approximately half of adolescents and adults newly infected with EBV will become symptomatic with IM. (9) The male to female ratio of cases is 1:1 although the age of IM is approximately two years younger in females in the United States.

EBV infection can mimic a number of clinical syndromes. Acute infection with EBV is easily confused with that of a streptococcal pharyngitis (which, in fact, may follow IM in a quarter of cases). Sore throat, fever, enlarged red tonsils with exudates, and easily palpable lymph nodes in the neck are all common features. Some differences do exist (for example, the lymph nodes are usually tender with streptococcal pharyngitis), but it can be important to make the distinction. Inadvertently treating IM with ampicillin (a typical antibiotic use in treating strep throat) results in the appearance of a maculopapular rash. In addition, the lymphadenopathy may raise cause for concern about the possibility of leukemia or lymphoma, especially when it is associated with lethargy and other non-specific symptoms.

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Non-nucleoside reverse transcriptase inhibitor (NNRTI) HIV treatment regimens are better at suppressing the virus than protease inhibitor (PI) regimens. Researchers used a meta-analysis to review 12 research trials comparing NNRTI to Pl, the two classes of antiretroviral drugs used in highly active antiretroviral therapy.

Virological suppression (as measured by CD4 count), death, disease progression, and withdrawal due to side effects were analyzed. NNRTI was up to 60% more likely to suppress …

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Abstract

Cucumber mosaic virus (CMV) causing mosaic and chlorosis of banana in Marthwada region was characterized on the basis of biological, serological and RT-PCR amplification of Coat protein. Mechanical inoculation tests, the virus was found to infect members of chenopodiaceae, Cucurbitaceae, Fabaceae, and Solanaceae. Partially purified virus preparations revealed the presence of isometric particles of 28nm in the electron microscopy. Insect vector transmission of CMV has indicated that Aphis gossypii was more efficient than A. craccivora in transmitting CMV in a non persistent manner. Using DAS ELISA CMV could be efficiently detected in different banana sample which are both symptomatic and symptom less plants. This would help in development of diagnostic tool for identifying and certifying planting material to check spread of disease.

Keywords: Banana, Chlorosis disease, Cucumber mosaic virus, ELISA detection, RT-PCR amplification

Introduction

Banana is an important fruit crop grown throughout the country. Banana crop is vulnerable to many diseases; among these viral diseases are the major production constraints. Infectious chlorosis disease of banana was first reported in Australia (Magee, 1940) and later in South and Central America, the Caribbean, India and the Philippines (Bouhida and Lockhart, 1990, Joshi and Joshi, 1974, Mali and Deshpande, 1976, Palukaitis et al., 1992). Banana chlorosis or heart rot disease has been reported to be caused by cucumber mosaic virus (CMV) (Magee, 1940; Singh et al., 1995, Kiranmai et al., 1998).

Cucumber mosaic virus (CMV), a positive sense RNA plant virus with a tripartite genome, is the type member of the genus Cucumovirus. CMV has a world -wide distribution and exists as a variety of isolates that differ in host range and pathogenicity (Palukaitis et al., 1992). CMV causes great losses in vegetables, ornamentals and fruits, and it is destructive due to its rapid spread by more than 60 aphid species in the field (Palukaitis and Garcia-Arenal, 2003). Transmission through planting material is also significant in some crop and weed hosts (Hsu et al., 2000). A number of CMV isolates have been described previously and classified into two subgroups, I and II, according to serological relationships, peptide mapping of the coat protein (CP), nucleic acid hybridization and nucleotide sequence identity (Palukaitis et al., 1992). More recently, phylogenetic analysis of a number of CMV isolates led to a further subdivision of subgroup I into subgroups IA and IB (Roossinck, 2002; Roossinck et al., 1999).

In India occurrence of CMV has been reported from many hosts. However, only limited reports are available on biological and molecular characteristics of these isolates (Madhubala et al., 2005, Verma et al., 2005,2006). CMV causes chlorosis, mosaic and heart rot in banana and has been found in most banana growing areas of the world. Infectious chlorosis disease of banana oftenconfused with zinc deficiency and or with the symptoms of Banana streak virus. Therefore the present investigations wereundertaken to identify the causal virus prevailing in Marthwada region based on transmission, serological testing and RT-PCR amplification.

Materials and Methods

Collection and maintenance of virus culture: Survey was conducted in Parbhani and Nanded districts of major banana growing areas of Marathwada region for the incidence of virus disease. Viral incidence was recorded based on symptoms observed on plants The symptomatic samples collected were tested by DAC-ELISA using CMV antisera and the samples which are positive to CMV were mechanically inoculated to Cucumber and the virus cultures were maintained for further studies.

Mechanical transmission and host range of virus</p>

Fort transmission and host range studies, mechanical inoculations were carried out by extracting infected leaf tissues in 0.1 M phosphate buffer, pH 7.0 containing 1.0% sodium sulphite (1:2W/V). Crude sap was inoculated mechanically on a number of test plant species of five plants each and inoculated plants were observed for one month for the appearance of symptoms. The plant species which are tested for host range are Cajanus cajan, Capsicum annuum, Chenopodium amaranticolor, Cicer arietinum, Cucumis sativus, Cucurbita pepo, Glycine max, Lycopersicon esculentum, Nicotiana glutinosa, N. tabacum, Phaseolus vulgaris, Vigna mungo, Vigna radiata, and Vigna unguiculata. Symptoms were recorded and checked for the presence of virus by backinoculation on to C. amaranticolor and by ELISA.

Aphid transmission of the virus</p>

For aphid transmission tests, Aphis gossypii was used with a preacquisition starvation period of 2 h, acquisition access period of 2 min and an inoculation period of 1 to 2 h on 8 plants of Nicotiana tabacum. The inoculated plants were observed for symptom development and presence of virus is confirmed by back inoculation on C. amaranticolor.

Virus Purification

The virus was propagated on N. glutinosa plants by mechanical inoculation. Leaves of N. glutinosa harvested three weeks after inoculation was used for purification. Purification was also done from virus infected banana samples by the method described by Tomlinson et al., (1973) with some modification. The inoculated leaves (100 g) were harvested after 4-5 days of virus inoculation and ground in 0.1 M citrate buffer, pH 6.5 in the ratio 1: 3 (w/v). Differential centrifugation was followed for purification of the virus.

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The last month of 2006 did not bring any substantial changes to the assortment of viruses found in the email traffic. Although analysis of the results for the entire year will be performed later, we can state that the Warezov worm family won a clear-cut victory in the autumn and winter months.

In December Warezov variants took the three top positions in the rankings, while the traditional change of leader turned into a family affair: Warezov.fb replaced Warezov.gj. We had expected and predicted this change: in December the former leader’s ranking declined sharply as it yielded …

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Over the past few decades, there has been a dramatic increase in the rate of emergence and re-emergence of infectious diseases. (1,2) While some diseases did not infect large numbers of people or have high mortality rates, they had economic consequences. Infections from the SARS virus, for example, resulted in under 1,000 deaths, but caused an estimated 2% decline in gross domestic product in East Asia.

A pandemic influenza outbreak could result in the loss of millions of lives and cost an estimated 900 billion dollars (U.S. currency). We have observed the purposeful release, in …

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TUCSON, ARIZ. — Preliminary results from a genomic study of patients infected by the hepatitis C virus suggest that a polymorphism in the interferon receptor promoter region could be a biomarker for predicting who will develop depression when treated with interferon-based therapies and ribavirin.

The polymorphism, -408 C/T, was present in 23 of 60 patients, Dr. Muhamad Aly Rifai reported at the annual meeting of the Academy of Psychosomatic Medicine. All but two patients with the polymorphism developed depression. No patient without -408 C/T had the mood disorder.

"This is …

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Background & objectives: Rubella virus (RV) is one of the leading causes of childhood blindness in India. In this study we applied an optimized nested reverse transcription polymerase chain reaction (nRT-PCR) to detect RV in clinical specimens.

Methods: nRT-PCR was optimized using total RNA extracted from standard strain of RV using nested sets of primers specific for El open reading frame. nRT-PCR was applied onto 30 lens aspirates and corresponding peripheral blood leucocytes of 30 infants with congenital (29)/ developmental (01) cataract. Serology for anti-RV IgG and IgM antibodies was done. RV isolation was attempted using Vero and SIRC cell cultures.

Results: Optimized nRT-PCR was specific for RV and sensitive to detect 10 fg of RV RNA. Among 30 patients, nRT-PCR detected presence of RV in lens aspirates of 6 (20%) and 4 corresponding leucocytes. RV was isolated from 3 (10%) lens aspirates (nRT-PCR positive) of the 30 patients. Sera of these 6 patients showed presence of anti-RV IgG and IgM in one, only anti-RV IgG in 3 others and none in the other two. Of the remaining 24 patients, anti-RV IgG was detected in 3 and no anti-RV IgM antibodies in others.

Interpretation & conclusion: Findings of our study showed that the nRT-PCR was a more sensitive and rapid technique to detect RV from lens aspirates compared to conventional methods of virus isolation and serology.

Key words Congenital cataract - congenital rubella syndrome - lens aspirates - RT-PCR - rubella virus

Rubella virus (RV) is a non-arthropod borne RNA virus and is the sole member of the genus Rubivirus in the family Togaviridae. Rubella infection is generally mild with few complications, but when acquired by pregnant woman during the first trimester of pregnancy, the virus is transmitted to the foetus with 90 per cent chances of development of congenital malformations in the newborn1. Earlier studies have shown that 10 to 40 per cent of congenital cataract was due to RV associated cataract in India and these were based on serology, results of which are difficult to interpret1-5. Ocular consequences of congenital rubella syndrome (CRS) may clinically develop during or after neonatal period6. Since RV has been known to be shed for up to 1 to 3 yr in clinical specimens such as the cataractous lens, a positive virus culture in such specimens from neonates is diagnostic of congenital infection7. We had earlier studied the association of congenital cataract with RV based on virus isolation8. RV replicates in a wide range of cell lines producing subtle and slow developing cytopathic effect often difficult to visualize because of low multiplicities of infection and is detected by immunofluorescence or RTPCR9. A variety of PCR assays have been described for detecting RV genome directly from clinical samples10-15. In order to improvise the sensitivity of the detection rate, for the association of the virus to congenital cataract, an optimized nested RT-PCR was applied to detect RV in lens aspirates and peripheral blood samples of infants with congenital or developmental cataract.

Material & Methods

Patients & specimens: In this study over a period of 10 months (1st March to 31st December 2005) at the tertiary care ophthalmic hospital, Sankara Nethralaya, Chennai, lens aspirates and peripheral blood leukocytes obtained from 30 infants (

Serology: Serum samples from all the 30 patients were collected at varying periods of 2 days to 3 months prior to surgery and tested for the presence of anti-RV IgG and IgM antibodies by ELISA using BIO ELISA procured from BIOKIT, Barcelona, Spain, as per the instructions provided in the manual.

Isolation of rubella virus: Virus isolation was attempted by standard conventional test tube culture method7 using Vero cells (supplied by National Facility for Animal Tissue Culture, NFATCC, Pune, India) and Statens Serum Institute Rabbit Corneal Epithelial Cell line (SIRC) cells (provided by Dr Savithri Sharma, L.V. Prasad Eye Institute, Hyderabad)8.

Preparation of RNA: The lens aspirate specimens were extracted using Qiagen Viral RNA extraction kit procured from Qiagen, Hilden, Germany, as per the instructions provided in the manual. Extraction of RNA from the leucocytes was done using the standard guanidium thiocyanate protocol16.

Nested reverse transcription polymerase chain reaction (nRT-PCR): Rubella virus cDNA was generated using the one step RT-PCR kit (Qiagen, Germany). The reaction was performed in 50µl volumes as per the manufacturer’s instructions. The primer sequences for the I and II round of nRT-PCR are shown in the Table13. The enzyme mix facilitates both reverse transcription and polymerase chain reaction. The annealing temperature was optimized to 61°C as against 60°C in the original report12. Amplification of 143 bp produced in nested PCR indicated the presence of RV specific RNA. The sensitivity of the primers were determined by diluting the initial cell culture harvest 10-fold in Dulbeccos Minimum Essential Medium (DMEM), following which the RNA extraction was performed from each of the 10 log dilutions and nRT-PCR was set up for each. The specificity of the primers was determined by performing nRT-PCR using the RNA extracted from the following that commonly cause ocular infections and human DNA from peripheral blood leucocytes from healthy blood donors. The bacterial RNAs tested include Staphylococcus aureus (ATCC 25293, American Type Culture Collection, USA), Pseudomonas aeuroginosa (ATCC 7853, American Type Culture Collection, USA), Mycobacterium tuberculosis (H37Rv, Tuberculosis Research Centre, Chennai) and Chlamydia trachomatis serotype A (ATCC VR 517B). The virus RNAs tested include - Adenovirus serotype 2 (ATCC 846-VR, National Institute of Allergy and Infectious Diseases, USA), Herpes simplex virus-1 (ATCC 733 VR, Chemicon, USA), Cytomegalovirus (AD169, provided by Dr Sridharan, Christian Medical College, Vellore), Varicella zoster virus (Oka Vaccine strain - Varilix vaccine, Smithkline Becham, Belgium) and ECHO11 (provided by Dr Nalini Ramamoorthy, King Institute, Chennai). Fungus RNAs includes Candida albicans (ATCC, American Type Culture Collection, Ranbaxy, New Delhi) and Aspergillus flavus (laboratory isolate).

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Massive Multi-Variant Malware Signals a Challenging 2007 for Traditional Anti-Virus Solutions

MOUNTAIN VIEW, Calif. — Spraying across the Internet in celebratory viral "confetti," the email-borne "Happy New Year!" malware outbreak circumvents many leading signature-based AV solutions, Commtouch (Nasdaq: CTCH) reported.

The ‘Happy New Year!’ malware attack - which is still in progress - is the most intensive outbreak of 2006, since it is comprised of a staggering number of distinct, low-volume variants, which were released from multiple sources simultaneously, and at short time intervals.

"This outbreak ushered out 2006 with a bang, while loudly forewarning the nature of viral outbreaks in 2007," said Haggai Carmon, Commtouch Vice President of Products. "During 2006, a growing number of massive server-side polymorphic outbreaks swarmed the Internet and successfully maintained a sizable lead of several hours to weeks ahead of traditional signature-based solutions. Examples of these include Feebs, Stration/Warezov and of course the ‘Happy New Year!’ malware to name just a few. What makes them so unique," Carmon continued, "is that they are released in a large number of distinct and short-lived variants, making it impossible to generate one signature or heuristic rule to effectively protect against them. In this way, malware writers maximize their chances of infecting the largest number of machines."

Commtouch identified and blocked 3,262 distinct variants during the first 65 hours of ‘Happy New Year!’ malware activity, and there were at least three time periods on Friday, December 29, when the malware accounted for nearly 12% of all global Internet email traffic. On Friday Commtouch tracked 842 distinct variants that were released to the Internet during a single five-minute period.

"We expect this trend to continue to grow in 2007, since server-side polymorphic outbreaks have become the most effective method to infiltrate through existing defenses," Haggai Carmon summarized. "Events like the New Year’s holiday force virus writers to concentrate their massive outbreaks in a short period of time. Other outbreaks like the Stration/Warezov attack can afford to stretch on for months, releasing recurrent waves of mass-variants each time."

The malware has been sent from multiple sources in a format that appears to be a New Year’s greeting, in order to entice users to open and click on the attachment. Subject lines of the messages include: "Happy New Year!" and "Happy 2007!" and sample attachment filenames are: postcard.txt, postcard.exe, or greeting card.txt. If a user opens the attached file, the malware attempts to shut down the PC’s security programs, scans for e-mail addresses to send out copies of itself, and installs various malicious programs that, among other things, turns the computer into a spam zombie.

Commtouch Zero-Hour[TM] Virus Outbreak Protection detects and blocks email-borne outbreaks like the "Happy New Year" malware within moments of their release, powered by its Recurrent Pattern Detection[TM] technology. Commtouch’s service is offered to messaging, security and anti-virus vendors for OEM integration as a complementary outbreak detection solution.

About Commtouch

Commtouch Software Ltd. (NASDAQ: CTCH) is dedicated to protecting and preserving the integrity of the world’s most important communications tool — e-mail. Commtouch has over 15 years of experience developing messaging software and is a global developer and provider of proprietary anti-spam and Zero-Hour virus protection solutions. Using core technologies including RPD (Recurrent Pattern Detection[TM]), the Commtouch Detection Center analyzes billions of email messages per month to identify new spam and malware outbreaks within minutes of their introduction into the Internet. Integrated by more than 50 OEM partners, Commtouch technology protects thousands of organizations, with over 50 million users in over 100 countries. Commtouch is headquartered in Netanya, Israel, and has a subsidiary in Mountain View, Calif. For more information, see: www.commtouch.com. The site includes the Commtouch online lab detailing spam statistics and charts.

This press release contains forward-looking statements, including projections about Commtouch business, within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. For example, statements in the future tense, and statements including words such as "expect," "plan," "estimate," "anticipate," or "believe" are forward-looking statements. These statements are based on information available to us at the time of the release; we assume no obligation to update any of them. The statements in this release are not guarantees of future performance and actual results could differ materially from our current expectations as a result of numerous factors, including business conditions and growth or deterioration in the Internet market, commerce and the general economy, both domestic as well as international; fewer than expected new-partner relationships; competitive factors, including pricing pressures; technological developments, and products offered by competitors; the ability of our OEM partners to successfully penetrate markets with products integrated with Commtouch technology; a slower than expected acceptance rate for our newer product offerings; availability of qualified staff for expansion; and technological difficulties and resource constraints encountered in developing new products, as well as those risks described in the text of this press release and the company’s Annual Reports on Form 20-F and reports on Form 6-K, which are available through www.sec.gov.

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