Part 2: Targeting a common virus to treat Multiple Sclerosis (MS)? The efforts to develop a vaccine against Epstein-Barr Virus (EBV) 

Writer: Emily DiMaulo-Milk

Editor: Joe Krzeski

            In April 2025, Moderna initiated a Phase II Clinical trial testing the investigational vaccine mRNA-1195 in patients with MS.1 This vaccine targets the common virus, Epstein-Barr Virus (EBV), which causes “mono”.2 A detailed explanation of the link between EBV and MS, as well as general background on both diseases, can be accessed at the first portion of this two-part blog post. Here, we will delve into the current standard of care for people living with MS and Moderna’s Horizon Trial.        

What are the current treatments available for Multiple Sclerosis and EBV?

            Multiple Sclerosis (MS) is a neurodegenerative autoimmune disorder which is caused by the destruction of the myelin sheath, a process called demyelination. The myelin sheath normally protects neurons from damage and enables speedy communication between neurons. Over time, as demyelination continues, the symptoms of MS can increase in severity and duration. There is currently no cure for MS, but there are many different medications available which can improve quality of life for people living with MS.3

The treatments for MS can be subdivided into two categories: treatments targeting symptoms (Table 1) and disease-modifying therapies (DMTs) (Table 2).4,5

What are some of the therapies which target the symptoms of MS?

During a severe flare up, a person may be prescribed corticosteroids such as oral prednisone or intravenous methylprednisolone to reduce inflammation. If these treatments are ineffective, plasma exchange may instead be used to treat severe symptom flare-ups. During plasma exchange, blood is removed from the body and separated into cells and a liquid component called plasma. The original plasma is replaced with plasma from healthy donors. The filtered blood is then returned to the body. Plasma exchange takes multiple hours and typically needs to be done several times to be effective.4,5 Anybody who meets the minimum requirements can help people living with MS by donating plasma, which can be accessed at the American Red Cross website. 

Outside of severe flare-ups, people living with MS may experience symptoms that impact their day-to-day functioning. Physical therapy can improve a host of symptoms, including bladder control, muscle strength and flexibility, and mobility. There are also accessibility tools which help people living with MS to adjust to changes in vision and physical ability. Occupational therapy can direct patients to resources and teach them how to use these tools. Outside of therapy, muscle relaxants such as baclofen (Lioresal, Gablofen) and tizanidine (Zanaflex) or onabotulinumtoxin A (Botox) can reduce muscle contractions. Onabotulismtoxin A (Botox) can also be used to treat any impairments in bladder control and reduce feelings of stiffness and involuntary muscle spasms. Dalfampridine (Ampyra) may be used to increase walking speed. Fatigue, one of the most common symptoms of MS, may be treated by stimulants such as methylphenidate (Ritalin, Concerta), though there is evidence that these medications may not be as effective as previously thought. Antidepressants such as bupropion (Wellbutrin) may be more effective and help with depressed mood, another common symptom of MS.4,5  

Table 1: Examples of treatments for MS which aim to improve symptoms.

TreatmentEffect
Corticosteroidsprednisone, methylprednisoneReduced inflammation during episodic flare-ups
Plasma exchangeImprovement of flare-up, used if corticosteroids are insufficient
Physical therapyCatered to the patient and can improve many symptoms
Occupational therapyEducates and directs patients towards accessibility tools
Muscle relaxants,Baclofen (Lioresal, Gablofen)     Tizanidine (Zanaflex)Reduced muscle contractions
Onabotulinumtoxin A (Botox)Reduced muscle contractions, stiffness, and spasmsImproved bladder control
Dalfampridine (Ampyra)Increased walking speed
StimulantsMethylphenidate (Ritalin, Concerta)Reduced fatigue, unclear effectiveness
AntidepressantsBupropion (Wellbutrin)Reduced fatigue, improved mood

What disease-modifying therapies (DMTs) are available and how do they work?

DMTs aim to slow or block the progression of MS by reducing the occurrence of demyelination. Because of this, DMTs are most effective at the early stages of MS. However, while these DMTs can be beneficial, they often cause significant side effects and thus must be used with caution.4,5

Demyelination in MS is driven by immune cells, called B- and T-cells, which mistakenly target the cells which make up the myelin sheath. Some DMTs broadly target inflammation, such as interferon-beta medications and glatiramer acetate, to dampen the immune response. Other DMTs aim to act directly upon immune cells. Teriflunomide (Aubagio) targets a type of metabolism that activated immune cells are particularly dependent upon.6 Fingolimod7 and Natalizumab8 are two different medications that both block immune cells from migrating to the brain, where demyelination occurs. One of the most widely prescribed DMTs are anti-CD20 monoclonal antibody therapies, such as Ocrelizumab and Ubituximab. Anti-CD20 monoclonal antibodies bind to B-cells, which causes other immune cells to kill the bound B-cell.4, 5 In many ways, this is similar to the demyelination process. However, these treatments are helpful because the cells which are depleted are those that produce the autoreactive antibodies which bind to the myelin sheath. 

Overall, MS can have many different symptoms and affect people in different ways. The symptoms of MS can be transient or persistent and new symptoms may develop as the disease progresses. There are also multiple types of medications that target the same symptom or biological event. Every treatment has different side effects and effectiveness from person to person. Therefore, patients and doctors closely work together to determine the appropriate medications on an individual basis. It may take a long time to find the best combination of medications for a person. 

Table 2: Examples of disease-Modifying Therapies (DMTs) to slow or stop the progression of MS.

TreatmentEffect
Interferon-beta medicationsBroad suppression of immunity and inflammatory response
Glatiramer acetateBroad suppression of immunity and inflammatory response
Teriflunomide (Aubagio)Inhibition of activated immune cells by hindering their metabolism
Fingolimod, NatalizumabBlockade of infiltration of immune cells into the brain
Anti-CD20 Monoclonal AntibodiesOcrelizumab, UbituximabDepletion of B-cells which drive demyelination

Are there treatments or preventatives which target Epstein-Barr Virus (EBV)?

In the previous blog post, we described the evidence for a link between MS and Epstein-Barr Virus (EBV) and background on this common virus. It is possible that any treatments which are effective against this virus would also be effective against MS. 

EBV is also the virus which causes infectious mononucleosis, or “mono,” an acute viral infection characterized by swollen lymph nodes, rash, fatigue, sore throat, and fever. Treatment for mono consists of rest, plenty of fluids, and over-the-counter antipyretics like ibuprofen. In people who are immunocompromised, acyclovir or ganciclovir may be used to prevent the uncontrolled lytic replication of herpesviruses, including Epstein-Barr Virus.2 These medications work by blocking the virus from making more copies of the viral genome during the lytic phase. However, this medication is not specific to EBV and does not affect the virus during the latent phase of infection.9 Interestingly, anti-CD20 monoclonal antibody therapies are commonly used to treat EBV-associated B-cell Lymphomas. The virus typically infects CD20-expressing B-cells,2 and the application of anti-CD20 monoclonal antibodies in people living with MS may also affect cells which are infected with EBV. 

Currently there are no EBV-specific treatments available. There have been many efforts to develop a vaccine to protect against infection with EBV, but none of them have been successful in practice.10

How would a vaccine help people already infected with EBV?

How would a vaccine against EBV work?

During an infection, specialized immune cells will develop an ability to recognize and respond to motifs which are specifically associated with the presence of a pathogen, called antigens. This is a normal part of a healthy immune response, called adaptive immunity. Adaptive immunity is extremely important for the successful resolution of an infection, and it protects against reinfection with the same pathogen. Vaccination exposes the immune system to an antigen to “train” the adaptive immune system to recognize and respond to that antigen without getting sick in the first place. There are many kinds of vaccines- some of which use strains of a pathogen which do not cause sickness and others that contain an antigen or cause the expression of antigen. However, regardless of the type of vaccine, a successful vaccination will result in the development of antibodies against and immune cells which recognize the antigen which was present in the vaccine.

Conventionally, vaccination has been used as a prophylactic, or a treatment which would prevent a person from getting infected. Vaccines against EBV have been designed for this application and have historically been unsuccessful. However, researchers have recently released the broader potential of vaccination as a method of harnessing the body’s endogenous ability to kill dangerous cells. Cancer vaccines have been successfully applied in preclinical models, where an antigen which is specific to the tumor is injected to improve the ability of the immune system to kill cancer cells.12 Applying a vaccine against EBV to someone already infected with EBV would work in a similar way; rather than preventing someone from becoming infected with EBV, it would enable immune cells to recognize and kill cells that express an antigen associated with EBV. 

A critical consideration in vaccine design is the selection of which antigen(s) to target. Importantly, in healthy people, EBV is maintained in the deepest stage of latency, called Latency 0, where there is virtually no production of viral antigens.2 It is difficult to imagine a vaccine capable of inducing immunity against cells where EBV is in Latency 0. In the lytic phase and other stages of latency, there are many EBV antigens could be used in a vaccine. During the lytic phase, the virus induces the expression of over 80 proteins.13 In contrast, even during the most active stage of latency, there are only 9 viral proteins which are expressed. When considering which latency proteins to target, EBNA1 would likely be excluded as a candidate antigen in a conservative approach to vaccine design. This is due to the molecular mimicry of EBNA1 and the myelin sheath, though anti-EBNA1 antibodies are detectable in people without MS, making it unclear exactly how risky vaccination with an EBNA1-based antigen would be in practice.14Besides EBNA1, there are eight other EBV latency proteins which could be targeted. These are the proteins EBNA2, EBNA-3A/B/C, and EBNA-LP, which are all expressed in the nucleus of the cell. LMP1 and LMP2A/B are expressed on the surface of the cell, which is exposed to immune cells, and thus these proteins would theoretically be prime candidates for vaccination targets, but the biological effect and structure of these proteins complicate matters.2Overall, while there are just nine EBV latency proteins which could be targeted via vaccination, currently there is no consensus on which protein is the optimal immunogenic target. 

How could a vaccine against EBV help people living with MS?

Generally, a successful vaccination against EBV would either prevent initial infection with EBV or kill cells which are infected with EBV. The mechanism of how EBV contributes to the development and progression of MS remains unclear. Therefore, it is impossible to know exactly how a vaccine against EBV would help people who already have MS. Additionally, vaccines may have different effects dependent upon which antigen(s) are selected. 

In one proposal, autoreactive antibodies against the EBV protein EBNA1 also target the myelin sheath and cause demyelination to occur. In the later stages of latency and the lytic phase, expression of EBNA1 is magnified, which would promote the activation and proliferation of immune cells which are responsive to EBNA1. Cells which make up the myelin sheath could be bystanders that are increasingly destroyed as immune cells initiate a response to EBNA1.15,16 EBV infection may promote sustained, low-grade inflammation against many different viral antigens which promotes the development of autoimmune disease.15 Vaccination against a viral antigen which is produced during later, more active stages of latency could reduce the scale of a pro-inflammatory event by triggering a more rapid and complete response to the virus. 

Recent research using cells isolated from people with MS during a disease flare-up suggests that people with MS may have dysregulation of the lytic phase of EBV.17 Pro-inflammatory signaling proteins, called cytokines, are produced by host cells in response to the virus. If the lytic phase of EBV is important in MS progression, a vaccine which targets lytic EBV could reduce MS flare-ups or slow disease progression by reducing the scale of lytic reactivation and the associated production of pro-inflammatory cytokines. 

Another potential mechanism for the association between EBV and MS is explained by the discovery that cells infected with EBV can escape the biological processes which normally prevent the survival of immune cells that recognize self-antigen.18 These EBV-infected cells could then activate even uninfected immune cells to cause a cascade of aberrant inflammation which drives autoimmune disease. In this case, vaccination against a viral antigen would be impactful because it would kill the cells which respond to self-antigen and drive demyelination. However, if these cells are in Latency 0, it is unlikely that vaccination against EBV would be a successful treatment on its own.

While researchers don’t yet fully understand how EBV contributes to the development and progression of MS, if a vaccine against EBV proves to have therapeutic value to people living with MS, it is not critical to understand exactly how the vaccine works. In fact, there are many FDA-approved medications, including some of the treatments for MS, which are incompletely understood. Rather, scientists can continue their research to better understand and develop improved treatments for MS while people living with MS benefit from any effective and safe treatments. 

Who else could potentially benefit from a vaccine against EBV?

            EBV has been linked to many different autoimmune disorders. These include Systemic Lupus Erythematosus, Rheumatoid Arthritis, Sjögren’s syndrome, and others. However, EBV was first identified as an oncogenic virus and continues to drive the development of many cancers. These include the Burkitt Lymphoma, Diffuse Large B-Cell Lymphoma, NK/T- cell Lymphoma, Gastric Adenocarcinoma, Nasopharyngeal Cancer, and many other cancers. In fact, an estimated 1.3-1.9% of all cancers worldwide can be attributed to EBV.2 Therefore, a vaccine which prevents EBV infection or selectively kills EBV-infected cells has the potential to benefit millions of people with many different diseases. 

What are the details of the ongoing Moderna clinical trials testing EBV vaccines?

Currently, Moderna is performing three different clinical trials to test two different vaccines against EBV, mRNA-1195 and mRNA-1189. In April 2025, Moderna initiated the Horizon Trial, a Phase II clinical trial testing mRNA-1195 in people with Multiple Sclerosis.1 Simultaneously, mRNA-1195 is being tested in healthy adults in a Phase I clinical trial, the Equinox Trial, which was initiated in 2023 and is currently active but no longer recruiting.19 mRNA-1189 is being tested in the Eclipse Trial, where it is currently in Phase I/II development to adolescents aged 10-21.20

What are the mRNA-1195 and mRNA-1189 vaccines?

In 2021, Moderna announced the development of the mRNA-1195 and mRNA-1189 vaccines targeting EBV. mRNA-1195 was intended to be used in people already infected with EBV while mRNA-1189 was developed as a prophylactic vaccine to prevent EBV infection. 21 Both vaccines are mRNA vaccines which act by inducing the expression of the antigen in a person’s cells. The most widely known application of mRNA vaccines are vaccines against COVID, such as the one developed by Moderna, though mRNA vaccines have been in clinical trials since 2013.22 mRNA-1189 and mRNA-1195 both contain antigens for five different EBV lytic proteins23,24 and mRNA-1195 contains additional antigens from undisclosed EBV latency proteins.24

The antigens contained in the vaccine, gH, gL, gB, gp42, and gp350 are expressed in cells during the lytic phase but primarily are on the surface of the virus, or the EBV envelope. EBV relies on these proteins to initially infect a cell. They bind to host proteins on the cell surface to triggere the engulfment of the virus or fusion of the EBV envelope with the cell.2 Antibodies against these viral proteins physically block the interaction of these viral proteins with host proteins on the surface of the cell, thus blocking EBV from entering the cell to establish infection. 

Historically, vaccines against EBV have largely targeted the lytic protein gp350.10 However, while gp350 is abundantly expressed on the surface of EBV, it has proven to be unsuitable as a singular target for vaccination.10 This is likely because EBV infects both epithelial and immune cells, but relies on different viral/host protein interactions to enter the cell. The EBV proteins gp350 and gp42 interact with host proteins primarily expressed by immune cells and generally not expressed by epithelial cells. Resultingly, vaccination against gp350 or gp42 may protect B-cells from infection with EBV but it does not block the infection of epithelial cells. Excitingly, mRNA-1189 and mRNA-1195 also contain additional antigens against the viral proteins gH, gL, and gB. These proteins are critical for the infection of both epithelial and immune cells.2 Therefore, mRNA-1189 and mRNA-1195 both improve upon the historical standard by incorporating antigens which are important for epithelial cell infection.

What are the details of the Horizon Trial for mRNA-1195 in people with MS?

The Horizon Trial is currently recruiting an estimated 180 people between the ages of 18-55 with MS who are willing to undergo vaccination with mRNA-1195. The study will assess the safety, tolerability, and efficacy of the vaccine at controlling EBV infection as well as its therapeutic potential for preventing disease relapse in people living with MS. The trial will last approximately 30 months. Each person will receive three injections with either the vaccine or a placebo in their upper arm. Two different doses of the vaccine will be tested on a 0-, 2-, and 6-month schedule. 

The efficacy of the vaccine will be determined by quantifying the in antibodies which neutralize B-cells and/or bind to the antigen of the vaccine. Both the abundance of antibodies and the change in antibody levels over time will be assessed. To determine the ability of the vaccine to block relapse, MRIs will be performed to detect the presence of new or worsening lesions in the brain and the time between MS flare-ups compared between the group which is vaccinated and the group which received the placebo. Patients will also undergo neurological exams to measure the severity of MS symptoms. The estimated primary completion date is in January, 2029.1

Both the Equinox and Eclipse trial are estimated to reach completion later this year, in October, 2026.19, 20 The results of these studies, which are focused just on the safety, tolerability, and efficacy of the mRNA-1195 and mRNA-1189 vaccines, respectively, should also indicate if the Horizon trial has any promise.

Will a vaccine against EBV be effective?

Overall, while vaccination against EBV has therapeutic potential, there are many hurdles to the development of a vaccine. These include difficult decisions regarding what antigen(s) should be targeted by vaccination as well as questions of the actual efficacy of any vaccine. While the first EBV vaccine was in clinical trials over 30 years ago, so far, no EBV vaccine has been successful at preventing infection with the virus. However, a successful EBV vaccine has the potential not just to help people living with MS, but also to prevent millions of cancer cases and improve the lives of people with other autoimmune diseases, especially considering there are currently no EBV specific treatments available. Therefore, the potential benefits of an EBV vaccine make these investigations worthwhile, despite the historical difficulty in targeting this common virus.

Glossary:

Multiple Sclerosis (MS): A neurodegenerative disorder driven by autoimmune destruction of the myelin sheath. It is typically diagnosed in early adulthood. Symptoms are impaired motor and sensory function and are progressive. There is no cure for MS. 

Neurodegenerative disorder: A disease caused by destruction of neurons.

Autoimmune disorder: A disease caused by abnormal activity of the immune system negatively impacting healthy cells.

Demyelination: The destruction of the myelin sheath and the physiological change which causes MS symptoms.

Myelin Sheath: The fatty coating along the axon which protects the axon from damage and allows the electrical signal to travel quickly without degradation.

Neurons: Specialized nerve cells which sense the environment, control muscle movement, and are responsible for communication between the brain and the body.

Disease Modifying Therapies (DMTs): Treatments which aim to stop the progression of a disease by targeting the underlying cause.

Plasma: The liquid component of blood which contains soluble factors that can promote inflammation.

B-cell: A type of immune cell which produces antibodies and plays a supportive role in immunity. Also the type of cell that EBV primarily infects.

T-cells: A specialized immune cell, most well-known as the cells which monitor for dangerous cells, like a cancer cell or a virus-infected cell, by checking the proteins expressed in that cell.

Anti-CD20 Monoclonal Antibody Therapy: A treatment which is used to help people with MS as well as treat some B-cell Lymphomas, including one which are EBV-positive. These treatments target B-cells and result in their clearance by the immune system. 

Epstein-Barr Virus (EBV): A common virus which causes a lifelong infection and has been linked to many different cancers and autoimmune disorders. There are no EBV vaccines or specific treatments available.

Lytic: The phase of the viral lifecycle during which most viral proteins are produced and which, if successfully completed, results in the production of more virus. This phase is essential for the transmission of virus from person to person. 

Latent: The phase in the viral lifecycle where the virus is largely inactive. EBV spends the majority of its lifecycle in this phase.

Adaptive Immunity: An immune response which develops over a prolonged period of time that is specific to a particular antigen. The adaptive immune response blocks the same pathogen from reinfecting an organism and is also important in the effective clearance of an infection. Vaccines aim to produce an adaptive immune response.

Antigen: A substance which produces an immune response. In this context, an antigen is a component of a vaccine.

Prophylactic: A treatment which is given to prevent the development of a disease.

Latency 0: The deepest stage of EBV latency, during which there is virtually no production of viral proteins. In healthy people, the virus will persist in this stage of latency for the majority of the time.

EBNA1: A critical viral protein which enables the replication of the virus and the maintenance of the virus in a cell. Antibodies against this viral protein have been implicated in the development of MS.

Molecular mimicry: The phenomenon of a foreign antigen from an infectious agent having structural similarity to a protein normally produced in healthy cells. 

Latency proteins: In the context of EBV, the latency proteins are EBNA1, EBNA2, EBNA-3A/B/C, EBNA-LP, LMP1, LMP2A/B. 

Autoreactive: A descriptor for immune cells which recognize and react to self-antigen. They are associated with autoimmune diseases.

Cytokines: Compounds produced by the immune system which modulate the inflammatory response.

mRNA-1195: One of two EBV vaccines developed by Moderna and in clinical trials. mRNA-1195 contains antigens for undisclosed latency proteins and five lytic proteins which mediate the entry of EBV into a cell. This vaccine theoretically targets cells already infected with EBV if they exit Latency 0 as well as block the transmission of EBV. 

mRNA-1189: One of two EBV vaccines developed by Moderna and in clinical trials. mRNA-1189 contains antigens for five lytic proteins which mediate the entry of EBV into a cell. This vaccine theoretically blocks the transmission of EBV.

Horizon Trial: The Phase II Moderna clinical trial testing mRNA-1195 in people with Multiple Sclerosis. This trial is currently recruiting participants.

Equinox Trial: The Phase I Moderna clinical trial testing mRNA-1195 in healthy adults. This trial is active but no longer recruiting.

Eclipse Trial: The Phase I/II clinical trial evaluating mRNA-1189 in adolescents aged 10-21. This trial is active but no longer recruiting.

mRNA vaccine: A type of vaccine which contains “instructions” for a cell to produce an antigen rather than a segment of peptide, such as the Covid-19 vaccine produced by Moderna.

Lytic Proteins: In the context of EBV, there are over 80 proteins which are produced during the lytic phase. Most vaccines have targeted the lytic protein gp350, which EBV uses to attach to and then infect B-cells. mRNA-1189/1195 contain antigens for the lytic proteins gp350 and gp42, which mediate attachment and are involved in the infection of B-cells. They also contain antigens for the lytic proteins gH, gL, and gB, which mediate fusion of the EBV envelope with both epithelial cells and immune cells.

EBV envelope: A coating on the surface of the EBV virus which contains lipids (fatty chains) and proteins. During infection, the EBV envelope will fuse with membranes on the host cell which are made from the same material, allowing the core of the virus to enter into the cell and intiate infection. 

Epithelial cells: A broad term which refers to the class of cells that line the body and protect it from the environment. In the context of EBV infection, epithelial cells which are important are those of the tonsil, mouth, and stomach lining. 

References:

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