A virus spreads around and usually attaches itself to the host, multiplies & causes diseases. But is there something like an anti-virus? A single celled entity that does the opposite: spreads around 'kills' other viruses and/or cures diseases. Has anybody discovered something like it or is there any research group working on synthesizing one? If so any links to their publications? Forgive me if I got my facts wrong, I am physical sciences person and know nothing about biology. :)

  • $\begingroup$ The immune system is something that is fixed to the host organism and does not spread around in the atmosphere or water like a normal virus. $\endgroup$
    – MarcelineH
    Commented Jun 22, 2014 at 8:43
  • $\begingroup$ you could think of antibodies as "anti-viruses" (although they don't grow exponentially... $\endgroup$
    – TanMath
    Commented Dec 12, 2014 at 19:12

5 Answers 5


There is a "anti-virus," although many call it a virophage.In 2008, a paper in Nature was published about the observations of a new strain of a virus known as Acanthamoeba polyphaga mimivirus. This virus mainly attacks amoeba. It was discovered in 1992. It was one of the biggest viruses ever found.Later, a related virus called the mamavirus was discovered. But, after observing this specimen under an electron microscope, scientist found tiny viral particles attacking the mamavirus. It was called Sputnik. The Sputnik virus hijacks the mamvirus's machinery and depends on the mamavirus to survive. It made scientists wonder if the mamavirus is a living thing.

Here is a picture of it attacking the mamavirus:


You can see small subviral particles attacking the bigger virus. That is Sputnik. Note that it is a virus that coinfects other organisms but needs a virus infecting an organism to survive. According to Wikipedia:

Sputnik virophage is a subviral agent that reproduces in amoeba cells that are already infected by a certain helper virus; Sputnik uses the helper virus's machinery for reproduction and inhibits replication of the helper virus.

It seems that there are more species of virophages, including one that infects the marine phagotropic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus and another one known as the Organic Lake virophage but not much detail is known about this virus.

Here is the link to the Nature article on the Sputnik virophage, published in 2008:


It may be possible to synthesize one in the future. However using this to kill viruses would not make sense because the virophage technically still attacks the host of the virus it is hijacking, plus, from what I understand, it only uses the virus's machinery.

Hopefully this was helpful. If you have questions, you can comment on this answer...

  • $\begingroup$ +1 Thank you Abraham for sharing this! Have you found anywhere how many viruses the Sputnik can attack? I think it is unspecific, but some characteristics, it must have. $\endgroup$ Commented Dec 26, 2014 at 9:30
  • $\begingroup$ @Masi I didn't understand.. $\endgroup$
    – TanMath
    Commented Dec 27, 2014 at 19:29
  • $\begingroup$ Can Sputnik virus attack only some viruses? Which receptors does it have? $\endgroup$ Commented Dec 27, 2014 at 21:11
  • $\begingroup$ @Masi Sputnik only co-infects with one species.. About receptors, i don't know..it's probably in the nature article.. $\endgroup$
    – TanMath
    Commented Dec 28, 2014 at 21:55
  • $\begingroup$ Here one publication with good references to possible receptors plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0094923 We do not have currently enough tools to specify all the receptors of Sputnik virophage, I think. Only the tail protein has been used there. $\endgroup$ Commented Dec 28, 2014 at 21:58

There is no anti-virus to all viruses and there is no such anti-virus against a single virus yet, but there is immune response to virus. How efficient the immune response is then depends on many things. There is no perfect immune response. To develop such an antivirus that decreases viral load requires cooperation with the immune response. To develop such an antivirus is still in very very early stages, since we do not understand the fine regulation of many processes going on in the viral pathogenesis and how to stop them.

There exists in the nature some viruses that attack other viruses. However, we do not understand if they attack just one or two viruses. See Abraham's good answer here for the latest publications in Nature.

The immune response tries to eliminate the virus through antigen presentation and cell-mediated immune response. The humoral immune response works in the local sides where the cell mediated immune response does not reach. However, the immune response is sometimes (and often) insufficient to kill the virus.

To develop such a general anti-virus is difficult because of a variety of different viruses: (RNA vs DNA; positive sense vs negative sense; single strained vs double stranded; intracellular replication vs extracellular).

Here is an example of antigen presentation for HIV virus deduced from this answer:

enter image description here

where HIV infects the antigen presentation cells (APC) (dendritic cell and macrophages) and monocytes. It replicates actively in the lymphatic circulation. Since APCs are out, it is difficult to kill the virus. To develop such a general anti-virus against HIV would require very specific understanding of many things: probably, iPS cells and development of antigen presentation cells. My conjecture is to develop an APC cell that has receptor to HIV virus and so can reach it. However, only theory.

Gamma interferon should be included in the intersection between innate and adaptive immune systems. Interferons may play a central role in the future in the development of such anti-viral drugs, because they are specific. For instance, the activation of IFN-gamma stimulates the phagocytosis of macrophages against the mycobacteria tuberculosis which is facultatively intracellular (can be intracellular when necessary).

Innate and adaptive immune systems are visualised on the plane in the figure. You have then humoral immunity working around that plane as circles. I emphasize with that the local nature of humoral immune system and how it extends the cell-mediated immune system. Any attack on the heart of this system i.e. antigen presentation will also risk the humoral immunity and thus cause fast progression of the disease.

In summary, all measures that are used to decrease the viral load aim to target the immune system to express efficient way of decreasing the viral load (killing is just one of them!). This can be done through many ways - most of which we do not know much yet. iPS stem cell research and interferon research can be some good ways in the development of good anti-virals. However, this will take still many years (probably at least 40-50 years) to have enough control of the specific viral pathways.

  • 1
    $\begingroup$ Excellent, always like the use of a Venn diagram! $\endgroup$
    – Spinorial
    Commented Jun 22, 2014 at 16:14

But is there something like an anti-virus? A single celled entity that does the opposite: spreads around 'kills' other viruses and/or cures diseases. Has anybody discovered something like it or is there any research group working on synthesizing one?

Actually there is, it is called immune system. :-)

Most of the cells in your body have proteasomes, which can degrade proteins from the inside of the cell. The cells randomly choose sample proteins (possibly viral or cancer proteins) which are degraded by a proteasome into small 8-10 amino-acid length peptides. After that the cell chooses some of these peptides and send them to the endoplasmatic reticulum in where each of them meet with an MHC1 molecule (major histocompability complex) and binds to it. After that the cell sends the MHC1-sample complex to its surface. So every cell with nucleus has a lot of MHC1-randomProteinSample on its surface. These samples are checked an immune cell type called cytotoxic T-cells. These immune cells attach to the MHC1 of other cells using their TCR (T-cell receptor) and their CD8 coreceptor. The TCR has a part which consist of a random amino-acid sequence. Thanks to this random part it can recognize a very specific pattern of the small peptides which are bound to MHC1. So every cytotoxic T-cell is different and each of them can recognize a very specific pattern with its T-cell receptors. When a T-cell has a pattern match for the first time it waits for verification signal. It gets that signal on its CD28 receptor. The signal B7-protein is provided by a professional APC (antigen-presenting cell) which is infected by the virus or which phagocytized the virus, processed it, and now expresses it on MHC1 and MHC2 (MHC2 is similar to MHC1, but it can be found only on professional APCs). By virus infected APC the MHC1 can be enough to activate the cytotoxic T-cell. By not-infected APC the cytotoxic T-cell requires further help for activation. This help can be provided by a helper T-cell, which attaches to the MHC2 receptor and after the verification it sends the necessary cytokines to activate the cytotoxic T-cell. After the activation the cytotoxic T-cell can destroy every cell on which it finds an MHC1 with matching protein sample, and it can proliferate, so make many copies of itself. This whole process (activating the adaptive immune system) takes appr. 3-4 days. Until that the innate immune system holds the infection. The innate immune system is not so specific as the adaptive immune system, but it contains most of the APCs, so these two systems work together in order to defeat the infection. By the next infection there will be already active memory T-cells available, so the whole process will be much faster... This is shortly how a human immune response works by viral infections. Note that I left out the B-cell response against viral surface polysaccharides to stay short and simple. ;-)))

Synthetic drugs usually have a single active ingredient or just a few of them, so you cannot do an universal cure for viral infections because every virus is different. There are a few treatments already available (viral interference, receptor antagonists, viral enzyme inhibitors, RNA interference, etc...), but the most important thing is prevention due to vaccination (create memory T-cells by an infection with attenuated virus strains or by fooling the immune system with viral proteins, polysaccharides and some chemicals which kill a few cells). Probably in the distant future there will be nanobots which will be programmed to cure any type of viral infections and cancer, but with current technology that seems like a miracle...


Since most answers have already covered multicellular immune systems, I will try to explore the concept of unicellular immune systems.

The now famous CRISPR-CAS system originally evolved as a bacterial immune system to protect itself against phages.

enter image description here

Much like computer-based antivirus solutions, CRISPR CAS relies on a "signature" system.

Known targets for the CRISPR CAS system are encoded on bacterial DNA, and these known signatures are then transcribed and processed into short guide RNAs known as crRNAs.

These crRNAs are then used by the CAS protein complex to target and cut up (therefore inactivating) these DNA strands that match. This therefore allows the cells to possess a native antivirus system that can "receive live updates" just like a commercial software antivirus program by simply modifying their "signature list" of possible pre-crRNAs.

  • $\begingroup$ +1 for new idea. Can you please explore this topic a little more in relation to anti-virus. Now, your answer seems to be like from Wikipedia mainly. $\endgroup$ Commented Dec 28, 2014 at 22:02

Well, there are antiviral drugs that inhibit virus development. However, they are drugs, not cells but they can be quite effective in controlling diseases.

They are also quite available to the public and perhaps you (or someone close) have used them. For instance, Zovirax (acyclovir) is used in lip herpes.

Also, HIV therapy is used effectively to increase the life expectancy of AIDS patients.


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