Storm 2007 virus

Electronic greeting cards are highly suspect these days. Be wary of email with links to outlandish news stories. Instead, point your browser at your favorite news site.

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You are commenting using your Facebook account. Notify me of new comments via email. The body of this tag contains an encrypted string which contains the URL of the second-stage executable.

No files are ever transferred between hosts; the meta-tag and the result hash are the only things the trojan needs from the peers in order to find the download site. The DDoS attack is conducted by game4. It receives the target IP address and attack type by downloading a configuration file from a hard-coded website in the body of the trojan. The configuration file specifies the target by IP address only; the tool has no provisions to resolve DNS names to addresses.

In addition to the anti-spam sites we saw being attacked, the configuration file has also been seen containing IP addresses for websites associated with the Warezov virus - another spam system, probably operated by a competing spam group.

It seems that this spam group is prone to attack anyone that interferes with its business model, be it anti-spammer or spammer, or in some cases, third-party services. For example, one IP address being attacked was capitalcollect.

Following is a partial list of IP addresses seen targeted by the Storm Worm DDoS component during the time we were monitoring its control mechanism:. But it could also take another name from the contact list and place that address in the "From" field in the e-mail client.

It's called spoofing -- the e-mail appears to come from one source when it's really coming from somewhere else.

Spoofing an e-mail address accomplishes a couple of goals. For one thing, it doesn't do the recipient of the e-mail any good to block the person in the "From" field, since the e-mails are really coming from someone else. A Klez worm programmed to spam people with multiple e-mails could clog an inbox in short order, because the recipients would be unable to tell what the real source of the problem was.

Also, the e-mail's recipient might recognize the name in the "From" field and therefore be more receptive to opening it. It's important to have an antivirus program on your computer, and to keep it up to date. But you shouldn't use more than one suite, as multiple antivirus programs can interfere with one another.

Here's a list of some antivirus software suites:. Several major computer viruses debuted in In the next section, we'll take a look at Code Red. Both worms exploited an operating system vulnerability that was found in machines running Windows and Windows NT. The vulnerability was a buffer overflow problem , which means when a machine running on these operating systems receives more information than its buffers can handle, it starts to overwrite adjacent memory.

That means all the computers infected with Code Red tried to contact the Web servers at the White House at the same time, overloading the machines. That's because the worm creates a backdoor into the computer's operating system, allowing a remote user to access and control the machine. In computing terms, this is a system-level compromise , and it's bad news for the computer's owner.

The person behind the virus can access information from the victim's computer or even use the infected computer to commit crimes. That means the victim not only has to deal with an infected computer, but also may fall under suspicion for crimes he or she didn't commit. While Windows NT machines were vulnerable to the Code Red worms, the viruses' effect on these machines wasn't as extreme.

Web servers running Windows NT might crash more often than normal, but that was about as bad as it got. Compared to the woes experienced by Windows users, that's not so bad. Microsoft released software patches that addressed the security vulnerability in Windows and Windows NT. Once patched, the original worms could no longer infect a Windows machine; however, the patch didn't remove viruses from infected computers -- victims had to do that themselves. What should you do if you find out your computer has been hit with a computer virus?

That depends on the virus. Many antivirus programs are able to remove viruses from an infected system. But if the virus has damaged some of your files or data, you'll need to restore from backups. It's very important to back up your information often.

And with viruses like the Code Red worms, it's a good idea to completely reformat the hard drive and start fresh. Some worms allow other malicious software to load onto your machine, and a simple antivirus sweep might not catch them all.

Another virus to hit the Internet in was the Nimda which is admin spelled backwards worm. Nimda spread through the Internet rapidly, becoming the fastest propagating computer virus at that time. The Nimda worm's primary targets were Internet servers. While it could infect a home PC , its real purpose was to bring Internet traffic to a crawl. It could travel through the Internet using multiple methods, including e-mail.

This helped spread the virus across multiple servers in record time. The Nimda worm created a backdoor into the victim's operating system. It allowed the person behind the attack to access the same level of functions as whatever account was logged into the machine currently. In other words, if a user with limited privileges activated the worm on a computer , the attacker would also have limited access to the computer's functions.

On the other hand, if the victim was the administrator for the machine, the attacker would have full control. The spread of the Nimda virus caused some network systems to crash as more of the system's resources became fodder for the worm.

In effect, the Nimda worm became a distributed denial of service DDoS attack. Not all computer viruses focus on computers. Some target other electronic devices. Here's just a small sample of some highly portable viruses:. Next, we'll take a look at a virus that affected major networks, including airline computers and bank ATMs.

Many computer networks were unprepared for the attack, and as a result the virus brought down several important systems. The Bank of America's ATM service crashed, the city of Seattle suffered outages in service and Continental Airlines had to cancel several flights due to electronic ticketing and check-in errors. The progress of Slammer's attack is well documented. Only a few minutes after infecting its first Internet server, the Slammer virus was doubling its number of victims every few seconds.

Fifteen minutes after its first attack, the Slammer virus infected nearly half of the servers that act as the pillars of the Internet [source: Boutin ]. The Slammer virus taught a valuable lesson: It's not enough to make sure you have the latest patches and antivirus software.

Hackers will always look for a way to exploit any weakness, particularly if the vulnerability isn't widely known. While it's still important to try and head off viruses before they hit you, it's also important to have a worst-case-scenario plan to fall back on should disaster strike. Some hackers program viruses to sit dormant on a victim's computer only to unleash an attack on a specific date.

Here's a quick sample of some famous viruses that had time triggers:. Computer viruses can make a victim feel helpless, vulnerable and despondent.

Next, we'll look at a virus with a name that evokes all three of those feelings. The MyDoom or Novarg virus is another worm that can create a backdoor in the victim computer's operating system. The original MyDoom virus -- there have been several variants -- had two triggers.

One trigger caused the virus to begin a denial of service DoS attack starting Feb. The second trigger commanded the virus to stop distributing itself on Feb. Feline infectious peritonitis coronavirus FIPV is a well-known example of antibody-mediated enhanced uptake of virus in macrophages that disseminate and increase virus quantities that lead to enhanced disease [31] , [45].

Antigen-antibody complex formation with complement activation can also occur in that infection and some other coronavirus infections in animals. As a site proposed for testing vaccines in humans, we requested and were given approval for evaluating different vaccine candidates for safety and effectiveness.

The concern for an occurrence of lung immunopathology on challenge of mice vaccinated with an inactivated virus vaccine, as reported by Haagmans, et al. This finding was duplicated in an experiment reported here and was also seen in mice vaccinated with a range of dosages of a double-inactivated whole virus vaccine DIV and an rDNA S protein vaccine SV although the immunopathologic reaction appeared reduced among animals given the S protein vaccine when compared to those given the whole virus vaccine.

In later experiments, these findings were confirmed and the vaccine utilized by Haagmans, et al. Thus, all four vaccines evaluated induced the immunopathology; however, all four also induced neutralizing antibody and protection against infection when compared to control challenged animals.

The immunopathology in all experiments in the present study occurred in the absence of detectable virus in lungs of mice two days after challenge with infectious virus. In two experiments, a live virus group subsequently challenged with live virus was included.

Lungs of these animals revealed minimal or no histopathologic damage data not shown. These findings suggest that virus replication probably occurred early after challenge, including in animals given live CoV earlier, and is required for development of pathology, including for the immunopathology. Infection would have been transient, below the limit of detection two days after challenge, or neutralized in lung homogenates before testing for virus..

Nevertheless, the Th2-type immunopathology pattern was seen only in animals given an inactivated vaccine earlier. Those challenged animals exhibited infection similar to unvaccinated animals as well as Th2-type immunopathology. A similar experiment with a VEE vector containing only the S gene exhibited protection against infection and no immunopathology.

They attribute the immunopathologic reaction following these SARS-CoV vaccinations to presence of the nucleocapsid protein N in the vaccine. Virus infection was present in all groups after challenge but reduced in the S vector vaccine group. Histopathology scores were high for the N containing vector group and low for the S containing group and for the vehicle control group.

Eosinophilic infiltrates and IL-5 were increased in the N vaccine group but only IL-5 was increased in the S vaccine group. While increased titers of serum antibody were induced and no virus was detected day two after challenge in most animals, the Th2-type immunopathology occurred after challenge, and the immunopathology seen earlier after vaccination with the DI whole virus vaccine was seen again.

This experiment also included the whole virus vaccine tested earlier in ferrets and nonhuman primates where the Th2-type immunopathology was initially seen. That vaccine, the BPV in this report, exhibited a pattern of antibody response, protection against infection and occurrence of immunopathology after challenge similar to the DI whole virus vaccine DIV.

A final experiment was conducted to evaluate specificity. Challenge of animals given prior influenza vaccine were infected and exhibited histopathologic damage similar to animals given PBS earlier; neither group exhibited the eosinophil infiltrations seen in animals given a SARS-CoV vaccine.

In these various experiments alum was used as an adjuvant and this adjuvant is known to promote a Th2 type bias to immune responses [48]. However, the immunopathology seen in vaccinated-challenged animals also occurred in animals given vaccine without alum. In an effort to determine whether an adjuvant that induced a bias for a Th1-type response would protect and prevent the immunopathology, we initiated an experiment where the DI PBS suspended vaccine was adjuvanted with Freund's complete adjuvant, a Th1-type adjuvant.

However, this experiment was aborted by the September, , Hurricane Ike induced flood of Galveston, Texas. This adjuvant is thought to induce Th1-type immune responses [49].

The authors indicate no lung immunopathology was seen among animals after challenge, including the group given vaccine without adjuvant; however, whether the hamster model could develop a Th2-type immunopathology is uncertain. Finally, a number of other studies of vaccines in animal model systems have been reported but presence or absence of immunopathology after challenge was not reported.

A summary of the SARS-CoV vaccine evaluations in animal models including the current report that indicated an evaluation for immunopathology after challenge is presented in Table 2. As noted all vaccines containing S protein induced protection against infection while the studies with VEE and vaccinia vector containing the N protein gene only did not.

Also shown is that a Th2-type immunopathology was seen after challenge of all vaccinated animals when evaluation for immunopathology was reported except the study in hamsters with a GSK whole virus vaccine. Thus, inactivated whole virus vaccines whether inactivated with formalin or beta propiolactone and whether given with our without alum adjuvant exhibited a Th2-type immunopathologic in lungs after challenge.

As indicated, two reports attributed the immunopathology to presence of the N protein in the vaccine; however, we found the same immunopathologic reaction in animals given S protein vaccine only, although it appeared to be of lesser intensity.

Thus, a Th2-type immunopathologic reaction on challenge of vaccinated animals has occurred in three of four animal models not in hamsters including two different inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant.

An inactivated vaccine preparation that does not induce this result in mice, ferrets and nonhuman primates has not been reported. However, the evidence for safety is for a short period of observation. The concern arising from the present report is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the basis for developing a vaccine for SARS.

Additional safety concerns relate to effectiveness and safety against antigenic variants of SARS-CoV and for safety of vaccinated persons exposed to other coronaviruses, particularly those of the type 2 group. This concern emanates from the proposal that the N protein may be the dominant antigen provoking the immunopathologic reaction. As indicated, strong animal model evidence indicates expression of the N protein by SARS-CoV vector vaccines can induce sensitization leading to a Th2—type immunopathology with infection.

In contrast to our results, those studies did not find clear evidence of the Th2 type immunopathology on challenge of mice given a vector vaccine for the S protein. The finding of a Thtype pathology in our studies in animals immunized with an rDNA-produced S protein is unequivocal. In this regard, animal model studies with FIPV in cats and RSV in mice have indicated that viral surface proteins may be the sensitizing protein of inactivated vaccines for immunopathology with infection [32] , [45].

This suggests that presentation of the S protein in a vector format may direct immune responses in a different way so that sensitization does not occur. Limitations of the present studies include their performance in mice only and uncertainty of the relevance of rodent models to SARS-CoV vaccines in humans. Additionally, a more intense study for virus replication including quantitative RT-PCR assays might have confirmed the probability that virus replication is required for induction of the immunopathology after vaccination.

Evaluations of mechanisms for the immunopathology, including immunoglobulin and cytokine responses to vaccines and tests for antigen-antibody complexes in tissues exhibiting the reaction, could have strengthened the Th2-type immunopathology finding.

Finally, a successful study with a Th1-type adjuvant that did not exhibit the Th2 pathology after challenge would have confirmed a Th2 bias to immune responses as well as provide a potential safe vaccination approach for SARS.

We thank I. MBP antibodies were kindly provided by the laboratory of Drs. Competing Interests: The authors have declared that no competing interests exist. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. National Center for Biotechnology Information , U. PLoS One. Published online Apr Newman , 1 Tania Garron , 1 Robert L. Atmar , 3 , 4 Clarence J. Peters , 1 , 2 and Robert B. Patrick C. Robert L. Clarence J. Robert B.