Source: French to English Tester Published on: 2026-04-27
Source: The Conversation – France in French (3)– By Gaëtan Ligat, Lecturer, University of Toulouse; Inserm
Glioblastoma, a rare but aggressive cancer, resists treatments. Research has revealed the presence of cytomegalovirus, CMVH, a common virus in humans, in tumor cells. CMVH is not believed to be the cause of this cancer but may modulate its aggressiveness, according to the current hypothesis. And the study of interactions between glioblastoma tumor cells and CMVH opens new therapeutic perspectives.
Glioblastoma is thetumorthe most common cerebral and also one of the most aggressive in adults.
It is a glioma (that is to say, a tumor that develops in the brain or spinal cord) that grows rapidly. It develops from glial cells, these “support cells” of neurons in the shape of a star, calledastrocytesandoligodendrocytes.
A rare but aggressive cancer that resists treatments
This aggressiveness explains why, even when combining heavy treatments such as surgery, radiotherapy, and chemotherapy, the results often remain limited. This therapeutic difficulty is reflected in the numbers: although relatively rare (about 2 to 5 cases per 100,000 people worldwide), glioblastoma is associated with a very poor prognosis, with an average survival of about eighteen months after diagnosis.
Thus, its severity and the still insufficient effectiveness of treatments make it a major public health issue. For about twenty years, researchers have been exploring an intriguing lead: a virus very common in the population, human cytomegalovirus, could be present in these tumors. It could influence their development and contribute to their resistance to conventional treatments. A hypothesis that generates a lot of interest and opens the way to new therapeutic approaches.
Human cytomegalovirus: the virus that manipulates our cells
Thehuman cytomegalovirus(CMVH) belongs to the large family of herpes viruses, such as those responsible for cold sores or chickenpox.
It is a very widespread virus: in many countries, more than one in two adults have already been exposed to it. After the first infection, often without symptoms, the virus does not disappear. It remains present in the body in a “dormant” form, notably in certain blood cells. It can reactivate later, especially when the immune system is weakened.
What makes the CMVH particularly interesting isits ability to influence the functioning of the cells it infects. It can stimulate their division, help them escape programmed cell death, and alter the local immune response. All these effects could, in theory, promote tumor development and contribute to its resistance to treatments. CMVH is also the main cause of infection transmitted from mother to baby during pregnancy.
Detection of cytomegalovirus in glioblastomas
The first observations suggesting alink between CMVH and glioblastomasdate back to the early 2000s. Research teams then detected viral DNA as well as virus-specific proteins in brain tumor samples. These results opened up a new perspective: glioblastoma, already very complex biologically, could also be influenced by a common and persistent virus.
Since these first discoveries, numerous teams have confirmed the presence of HCMV in glioblastomas. The amount of virus detected remains low compared to an active infection, but even at these levels, it can produce proteins capable of influencing the behavior of tumor cells.
The presence of CMVH does not necessarily mean that it is the origin of the tumor. Although a study has shown thattransformation of human cells grafted into the mouse brain, the majority of data rather suggests that the virusacts as an “oncomodulator”A: it does not trigger tumor formation, but can modify its aggressiveness, certain biological characteristics, and amplify resistance to treatments.
The indirect role of the CMVH in glioblastoma progression: “oncomodulation”
CMVH does not appear to be the origin of glioblastoma, but it could modulate its aggressiveness through a phenomenon called “oncomodulation.” Unlike classical oncogenic viruses that cause cells to become cancerous, it does not directly induce the cancerous transformation of a healthy cell. Experimental data rather suggest that it acts on the tumor environment and on certain key mechanisms of cell biology.
Infection with HCMV can promote the formation of new blood vessels, allowing the tumor to receive more nutrients. It can also inhibit apoptosis, the natural process of eliminating abnormal cells, and interfere with major regulators of the cell cycle.
Moreover, the virus alters cellular metabolism to favor tumor survival and helps establish an immunosuppressive microenvironment, that is to say, one that reduces the effectiveness of the body’s defenses.
Together, these observations could strengthen the growth and resistance of glioblastomas. They also open upnew research perspectives and therapeutic strategies targeting not only the tumor but also its viral interactions.
Therapeutic implications
The discovery of CMVH in glioblastomas quickly led to the exploration of antiviral interventions as a complementary therapeutic approach.Pilot studies have tested valganciclovir, an antiviral treatment already used against CMV infections, in patients with glioblastoma. Although the results are still preliminary, some patients have shown a relative improvement in survival, suggesting that limiting the virus’s activity could slow tumor progression.
In parallel, research is turning to immunotherapeutic approaches targeting HCMV. The goal is to stimulate the immune system to specifically recognize and attack cells expressing viral proteins, thus offering a new avenue to treat a cancer that remains difficult to combat with conventional treatments.
The interest of these strategies goes beyond glioblastomas: the concept of “oncomodulator” virus could apply to other cancers, including some pediatric cancers such asmedulloblastoma, highlighting the possible role of congenital infection (infection transmitted to the baby before birth, during pregnancy, by the mother) in the modulation of the tumor. Moreover, CMVH was classified in 2025 as“probably carcinogenic to humans”(group 2B) by the International Agency for Research on Cancer (IARC), strengthening scientific attention on its effects on development and tumor progression.
Finally, in order to overcomethe emergence of resistances and the toxicity of classic treatmentsagainst CMVH, new innovative antiviral strategies are being explored. For example, ofsmall peptides designed to block the interaction between two essential viral proteins can inhibit CMV replication. This approach could complement, or even replace, classical antivirals.
A discreet virus that influences an aggressive tumor
CMVH perfectly illustrates how a discreet and very widespread virus can influence the biology of an aggressive tumor. In glioblastomas, its role as an “oncomodulator” does not consist in triggering the disease, but in amplifying its aggressiveness.
Studying this interaction opens new perspectives for better understanding and treating these difficult cancers, and shows the potential of an integrative approach combining virology and oncology.
Glioblastoma remains a major challenge, but research on CMV reveals that even seemingly silent viruses can help decipher the complexity of human diseases and offer new therapeutic strategies.
Gaëtan LIGAT is a member of the virology section of the French Society of Microbiology. He is also an administrator and scientific committee head of the association “Stars in the Sea, overcoming glioblastoma.” He has received funding from: the League Against Cancer, the Association for Research on Brain Tumors (ARTC), Stars in the Sea, overcoming glioblastoma, the Flavien Foundation, FONROGA, Growing up without cancer, Eva for life; Raphaël heart chocolate, 111 Des Arts Toulouse, the Occitanie region, Key Challenge CeBBOc, GEMSI.
–ref. Against glioblastoma, the most common brain tumor, the cytomegalovirus pathway –https://theconversation.com/against-glioblastoma-the-most-frequent-brain-tumor-the-track-of-cytomegalovirus-281280