By using our site, you agree to our cookie policy. Cookie Settings. Learn why people trust wikiHow. Download Article Explore this Article Steps. Tips and Warnings. Related Articles. Author Info Last Updated: January 2, Determine what operating system you are going to attack. The most common target is Microsoft Windows, especially older versions. Many old Windows users do not update their operating system, leaving them vulnerable to security holes that may be fixed in newer versions.
Mac OS X and Linux are both fairly virus-proof due to the way permissions work and the general architecture of the operating system. Decide how you want it to spread. A virus is only a virus if it can spread to other users. You will need to figure out the delivery method before beginning, as it is one of the fundamentals of the virus's code.
Common delivery mechanisms include: Executable file. COM etc. Macro Microsoft Office - Macros are programs that are embedded into a document or email.
They target Word, Outlook, and other macro-enabled products. The most common method of delivery is via email with an infected document attached. Web script - These are pieces of malicious code that are injected into sites without the webmasters' knowledge. Determine the weak spot that you want to target. Successful viruses exploit weak spots in a program's or system's security to spread and carry out their actions. This requires a lot of research and know how, but there are communities out there that can help you find what you need.
Decide what you want your virus to do. Once your virus has infected a system, what do you want it to do? Effects can range from nothing, to displaying a message, to deleting files, and much worse. Be aware that creating and spreading a malicious virus is a serious crime in the most countries.
Choose a language. In order to create a virus, you will need to have at least a basic understanding of at least one computer language or scripting tool. More complex viruses often involve several languages. For really effective viruses, you will need to be familiar with assembly languages. Sequence complementarity shared between the nucleotides within the cleavage site of the donor mRNA and the viral RNA facilitates successful cap snatching. The cap-stealing mechanisms used by segmented RNA viruses to generate their mRNAs circumvent this innate detection system.
Cap snatching of cellular mRNA. Downstream hairpin loops are RNA structures that facilitate initiation of cap-dependent translation in the absence of eIF2 translation initiation factors. In addition, the physiological state of the infected cell dictates whether host mRNA transcripts undergo cap-dependent translation or cap-independent translation.
When the cell exhibits normal housekeeping functions, translation of cellular mRNAs is carried out by a cap-dependent mechanism; however, under stressful conditions, such as heat shock, viral infection, hypoxia, and irradiation, the translation mechanism switches from cap dependency to IRES-driven mechanisms. Infection by a range of viruses induces the activation of the ER stress response, resulting in the stimulation of IRES-dependent translation.
As such, viruses containing IRES are able to efficiently benefit from the host cells ER stress response for their own multiplication. This is the site of binding of poly A binding protein in the cytoplasm. Viral mRNAs are synthesized without this signal sequence. Stuttering occurs at a site containing a slippery sequence mononucleotide repeats and involves 1-base repeated frameshifts on the mRNA strand Fig. Stuttering mechanism. This mechanism, also observed in some eukaryotes, allows RNA viruses except dsRNA viruses to produce multiple proteins from a single gene.
In these viruses, the RNA polymerase reads the same template base more than once, creating insertions or deletions in the mRNA sequence, thereby generating different mRNAs that encode different proteins.
There are two kinds of mRNA editing: 1 cotranscriptional editing through polymerase slippage and 2 posttranscriptional editing. RNA editing in members of the Ebolavirus genus increases their genome coding capacity by producing multiple transcripts encoding variants of structural and nonstructural glycoproteins from a single gene, ultimately increasing its ability for host adaptation.
Also observed in many cellular organisms, alternative splicing allows production of transcripts having the potential to encode different proteins with different functions from the same gene Fig. The sequence of the mRNA is not changed as with RNA editing; rather the coding capacity is changed as a result of alternative splice sites. Alternative splicing is regulated by cellular and viral proteins that modulate the activity of the splicing factors U1 and U2, both of which are components of the spliceosome.
Activation of the spliceosome is facilitated by cis-acting signals in the mRNA sequence. While only mature, spliced mRNA transcripts are exported out of the nucleus, hepadnaviruses and retroviruses are able to export nonspliced mRNA transcripts out of the nucleus for translation.
On the other hand, the NS1 protein n onstructural p rotein 1 of influenza viruses can interact with multiple host cellular factors via its effector- and RNA-binding domains. It is capable of associating with numerous cellular spliceosome subunits, such as U1 and U6 snRNAs, and can inhibit cellular gene expression by blocking the spliceosome component recruitment and its transition to the active state. Alternative splicing. Alternative splicing is common in parvovirus pre-mRNA transcript processing and allows for the generation of different proteins from a specific nucleotide sequence on the viral mRNA strand.
Dotted lines indicate alternative splice sites. Therefore, viruses can induce preferential induction of viral mRNA splicing by the cellular splicing machinery. Knowledge concerning the coordination between cellular and viral genome splicing comes from adenoviruses and retroviruses, but only limited data are available for other viruses, for example, influenza viruses.
This is also referred to as stop codon read-through, and is a programmed cellular and viral-mediated mechanism used to produce C-terminally extended polypeptides, and in viruses, it is often used to express replicases.
Termination of translation occurs when one of three stop codons enters the A-site of the small 40S ribosomal subunit. Stop codons are recognized by release factors eRF1 and eRF3 , which promote hydrolysis of the peptidyl-tRNA bond in the peptidyl transferase center P-site of the large ribosomal subunit. Read-through occurs when this leaky stop codon is misread as a sense codon with translation continuing to the next termination codon.
Read-through signals and mechanisms of prokaryotic, plant, and mammalian viruses are variable and are still poorly understood. Programmed ribosomal frameshifting is a tightly controlled, programmed strategy used by some viruses to produce different proteins encoded by two or more overlapping open reading frames Fig. Ordinarily, ribosomes function to maintain the reading frame of the mRNA sequence being translated. However, some viral mRNAs carry specific sequence information and structural elements in their mRNA molecules that cause ribosomes to slip, and then readjust the reading frame.
This ribosomal frameshift enables viruses to encode more proteins in spite of their small size. Ribosomal frameshifting. This occurs because the initiation codon can be part of a weak Kozak consensus sequence. As a result, there can be the production of several different proteins if the AUG codon is not in frame, or proteins with different N-termini if the AUGs are in the same frame.
A number of viruses engage in leaky scanning, including members of the families Herpesviridae , Orthomyxoviridae , and Reoviridae.
It is, therefore, referred to as cap-dependent discontinuous scanning. The mechanism of ribosome shunting has not been described in molecular detail. Shunting expands the coding capacity of mRNAs of viruses such as caulimoviruses. Ribosomal shunting.
Ribosomes, therefore, skip the synthesis of the glycyl-prolyl peptide bond at the C-terminus of a 2A peptide cleavage of the peptide bond between a 2A peptide and its immediate downstream peptide. Translation is then reinitiated on the same codon, which leads to production of two individual proteins from one open reading frame.
Viruses not only employ strategies that maximize the coding capacity of their small genomes, disguise their mRNA with the same structural elements found in host mRNA, regulate their genome expression in a time- and space-dependent manner, but they have also evolved ways of subverting host cell functions in order to favor their own replication and translation.
These phosphorylation events serve to activate or deactivate the enzyme. Some viruses herpesviruses, bunyaviruses counteract this phosphorylation at serine amino acids to inactivate RNA polymerase, while other viruses orthomyxviruses, togaviruses disrupt cellular RNA polymerase function by signaling ubiquitination of the enzyme and its subsequent degradation by proteasomal action.
Phosphorylation of serine residues located on the CTD of the enzymes is blocked by some viruses. Other viruses arrest RNA Pol activity by signaling ubiquitination of the transcribing enzyme, which is subsequently degraded by the proteasome. Viruses can engage in targeted disruption of cellular mRNA export pathways to promote preferential viral gene expression Fig.
All DNA viruses replicate within the nucleus except poxviruses, asfarviruses, and phycodnaviruses. Few RNA viruses, including bornaviruses, orthomyxoviruses, and retroviruses, replicate in the nucleus.
Trafficking between the nucleus and cytoplasm is usually unidirectional for large macromolecules like the mRNA transcript, and occurs through the n uclear p ore c omplex NPC.
Viruses that replicate in the nucleus must out-compete cellular mRNAs to export viral mRNAs out of the nucleus for translation into virus gene products in the cytoplasm. Several viruses can inhibit nuclear export of cellular mRNAs by disrupting nuclear export receptors exportin1 and TIP-associated protein and nucleoporins that comprise the NPC to compromise their function in nucleocytoplasmic trafficking of cellular mRNA.
One half of the NPC is shown in the diagram. Many DNA viruses e. Viruses have developed different strategies to effectively degrade host mRNAs and to allow preferential translation of their own mRNA Fig. Most viruses produce an endonuclease that cleaves host mRNAs, which are then degraded by host exonucleases e.
Betacoronaviruses, influenza viruses, vaccinia viruses, and herpesviruses can produce viral endonucleotyic products to an extent that saturates cellular RNA decay-related quality control mechanisms and limit their function. Transcripts of cytoplasmic viruses must circumvent the cellular mRNA decay machinery to enable virion production.
Picornaviruses are able to suppress cellular RNA decay factors, and polioviruses and human rhinoviruses produce viral proteases that degrade Xrn1, Dcp1, Dcp2, Pan3 a deadenylase , and AUF1decay factors. Viruses capable of inducing the shutdown of cellular mRNA translation are able to continue to translate at least part of their mRNAs using noncanonical translation mechanisms, for example, cap-independent translation, ribosome shunting, and leaking scanning e. Ransom0 is a open source ransomware made with Python, designed to find and encrypt user data.
Written in C. Generate Virus in Termux. RAT-el is an open source penetration test tool that allows you to take control of a windows machine. It works on the client-server model, the server sends commands and the client executes the commands and sends the result back to the server. The client is completely undetectable by anti-virus software. Add a description, image, and links to the virus topic page so that developers can more easily learn about it.
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