J. Microbiol. Infect. Dis., (2024), Vol. 14(3): 103–108

Review Article

10.5455/JMID.2024.v14.i3.3

Human immune responses to measles virus: A literature review

Balid Salim Albarbar^*

Department of Medical Laboratory, Higher Institute of Sciences and Medical Technology, Alkums, Libya

*Corresponding Author: Balid Salim Albarbar. Department of Medical Laboratory, Higher Institute of Sciences and Medical Technology, Alkums, Libya. Email: b.albarbar [at] yahoo.co.uk

Submitted: 01/06/2024 Accepted: 19/08/2024 Published: 30/09/2024

---

ABSTRACT

Measles disease is caused by the measles virus (MV), which is a highly contagious viral infection that mainly affects children. Measles disease is one of the vaccine-preventable diseases, despite the availability of an effective vaccine, measles remains a significant public health concern globally. Understanding the immune responses to the MV is very important for the development of improved vaccines and therapeutic strategies. The aim of the current study is to summarize current knowledge on the innate and adaptive immune responses to measles infection, including the role of various immune system components; cells, cytokines, and antibodies. In addition to that, the paper discusses the immunological memory generated following measles infection or vaccination and its implications for long-term protection.

Keywords: Measles virus, Immune system, Innate immune response, Adaptive immune response.

---

Introduction

The measles virus (MV) is a highly contagious virus belonging to the Paramyxoviridae family, genus Morbillivirus (de Vries et al., 2015). It affects the respiratory system and causes symptoms: fever, skin rash, cough, runny nose, and red eyes. Measles can lead to serious complications in young children and immune-compromised patients such as pneumonia, encephalitis, and leading to death (Laksono et al., 2016; Hübschen et al., 2022).

The MV is enveloped and spherical, with a single-stranded, negative-sense RNA genome. It contains six structural proteins, including the fusion (F) protein, hemagglutinin (H) protein, and matrix (M) protein (Bellini et al., 1994; de Vries et al., 2015). Measles is an airborne disease and spreads through respiratory droplets from coughing and sneezing. It can also be transmitted through contact with contaminated surfaces (Laksono et al., 2016). After inhalation, the virus infects the respiratory mucosa, spreads systemically via lymphatic and hematogenous routes, and causes a widespread rash due to the immune response (Wang et al., 2007; Gerlier and Valentin, 2009). Measles remains a significant cause of morbidity and mortality worldwide, particularly in low-income countries with limited access to healthcare and vaccination programs (Porter and Goldfarb, 2019). Despite the availability of a safe and effective vaccine, measles outbreaks occur periodically, often due to gaps in vaccination coverage. These outbreaks can result in high numbers of cases and strain healthcare systems (Rota et al., 2009).

Target cells of MV

MV primarily targets cells of the immune system and respiratory epithelium. Initial infection occurs in dendritic cells (DCs) and macrophages of the respiratory tract, facilitating dissemination throughout the body (Laksono et al., 2016). The virus then infects respiratory epithelial cells, where it replicates extensively. Subsequently, MV spreads to lymphoid tissues, including lymph nodes and tonsils, causing systemic symptoms (Lemon et al., 2011). Neurological complications can occur indirectly through immune-mediated mechanisms, reviewed in reference (Jain and Aulakh, 2022).

MV uses two cellular receptors to infect various types of cells. First, MV enters via a membrane cofactor protein known as CD46. CD46 receptor is expressed on a wide range of nucleated cells, including myeloid cells (such as DCs and macrophages), lymphoid cells (B cells and T cells), and epithelial cells. CD46 facilitates the entry of MV into these cells by binding to the hemagglutinin (H) protein of the MV (Lin and Richardson, 2016). Second, signaling lymphocyte activation molecule (SLAM), known as CD150. SLAM is primarily expressed in immune cells, including activated T cells, B cells, DCs, and macrophages. MV also interacts with SLAM through its H protein, allowing it to infect these immune cells (Lin and Richardson, 2016; Tatsuo et al., 2000).

These receptors play a crucial role in MV tropism, facilitating its ability to infect a broad range of cell types within the host. This dual receptor usage contributes to the systemic nature of measles infection and its ability to evade immune responses. Immunity to measles is mediated by two major parts of the immune system; innate and adaptive immune responses as discussed largely below.

Innate immune responses to MV

Innate immune responses are initiated in response to sensing by pattern recognition receptors (PRRs). PRRs are proteins expressed by cells of the innate immune system and are crucial for recognizing viral components called pathogen-associated molecular patterns, these receptors play a pivotal role in initiating immune responses against various pathogens (Bellini et al., 1994; Koyama et al., 2008; Gerlier and Valentin, 2009; Kawai and Akira, 2010).

Several PRRs are involved in detecting MV and initiating the immune response such as toll-like receptors; TLR2, TLR7, and TLR8 (Clifford et al., 2012; Zhou et al., 2021), Retinoic acid-inducible gene I-like receptors, NOD-like receptors, and C-type lectin receptors all play role in recognition of MV glycoproteins (Kawai and Akira, 2010; Zhou et al., 2021). Upon recognition of MV by PRRs, signaling cascades are initiated, leading to the activation of transcription factors such as NF-κB and IRF3/7 (Gerriets et al., 2016), which induce the expression of antiviral genes including type-I IFNs and pro-inflammatory cytokines secretion. These cytokines orchestrate the innate and adaptive immune responses for controlling MV infection and promoting viral clearance (Naniche, 2009).

Macrophages

Macrophages are among the first responders to MV infection. They recognize viral components through PRRs (Zhou et al., 2021). MV-infected cells release signals and pro-inflammatory cytokines, which activate macrophages. Activated macrophages phagocytose virus-infected cells and produce inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), contributing to the antiviral immune response. In order to undergo the phagocytosis process, antibodies facilitate the process of opsonization, where they bind to viral particles and mark them for destruction by immune cells such as macrophages and neutrophils through phagocytosis. This helps in the clearance of the virus from the body (Allen et al., 2018).

Dendritic cells

DCs play a crucial role in sensing MV infection and initiating adaptive immune responses. MV can infect DCs, leading to their activation and maturation. Activated DCs migrate to lymphoid tissues, where they present viral antigens to T cells, initiating adaptive immune responses against MV (Coughlin et al., 2013; Allen et al., 2018).

Natural killer (NK) cells

NK cells are called large granular lymphocytes, a type of innate lymphocytes that play a pivotal role in early antiviral defense (Caligiuri, 2008). MV infection induces the production of type-I IFNs and other cytokines, which stimulate NK cell activation. Activated NK cells recognize MV-infected cells through the release of cytotoxic granules containing perforin and granzymes that destroy infected cells (Griffin et al., 1990). Taken together, these cells of innate immune responses contribute to the control and clearance of MV infection, ultimately facilitating the resolution of MV. However, MV has evolved mechanisms to evade or suppress innate immune responses, leading to the characteristic immunosuppression associated with measles (Wang et al., 2007; Koyama et al., 2008; Griffin, 2010).

Complement system activation

The complement system is a series of proteins present in blood and play a major role in innate response to pathogens. The complement system enhances the destruction of virus-infected cells through processes like membrane attack complex formation and inflammation (Karp, 1999).

Secretion of pro-inflammatory cytokines

Various pro-inflammatory cytokines from innate immune cells (including macrophages and DCs) are secreted in response to MV infection and these include; IL-6, TNF-α, IL-1β, Type I interferons (IFN-α and IFN-β) and IL-12 (Gerlier and Valentin, 2009; Amurri et al., 2022). These play a central role in the acute-phase response and stimulate B cell differentiation. TNF-α, is produced mainly by macrophages and contributes to inflammation, apoptosis, and antiviral defense. It plays a critical role in orchestrating the immune response to MV. IL-1β, is produced by macrophages and other immune cells in response to MV infection. It promotes inflammation and activates endothelial cells, leading to increased vascular permeability. IFN-α and IFN-β are induced early during MV infection and have potent antiviral effects. They inhibit viral replication and enhance the expression of antiviral proteins. IL-12, is produced by antigen-presenting cells (APCs) such as DCs and macrophages. It stimulates NK cell activation and promotes Th1 cell differentiation, enhancing cellular immunity against MV (Gerlier and Valentin, 2009; Naniche, 2009; Amurri et al., 2022).

Secretion of chemokines

A number of chemokines are secreted in response to measles and these are including; CCL2, CXCL10, CCL5, and CXCL8 (Abt et al., 2009). CCL2 (monocyte chemoattractant protein-1, MCP-1) recruits monocytes and macrophages to the site of infection and promotes their activation. CXCL10 (interferon gamma-induced protein 10), CXCL10 is induced by IFN-γ and recruits T cells, NK cells, and macrophages to the site of infection. CCL5 (regulated upon activation, normal T cell expressed and secreted, RANTES), CCL5 attracts T cells, eosinophils, and basophils to the site of inflammation and contributes to immune cell activation. In addition to these chemokines, CXCL8 (interleukin-8, IL-8), is a potent chemoattractant for neutrophils and plays a role in the recruitment of these cells to the site of infection (Abt et al., 2009; Gerlier and Valentin, 2009; Naniche, 2009; Amurri et al., 2022). The production of these pro-inflammatory cytokines and chemokines during measles helps to recruit and activate immune cells, promote inflammation, and coordinate the antiviral immune response. However, dysregulated cytokine production can contribute to the immunopathology associated with severe measles cases, such as measles-induced immunosuppression or complications like pneumonia and encephalitis (Bellini et al., 2005; de Vries et al., 2012).

Adaptive immune responses to MV

T cell-mediated immunity plays a critical role in protecting against MV infection. When a person is infected with MV, both the innate and adaptive immune responses are activated. T cells, and B cells, are crucial components of the adaptive immune system and play several key roles in combating MV infection (Griffin, 2016). When the MV infects host cells, it triggers the presentation of viral antigens on the surface of infected cells. APCs, such as DCs and macrophages, then present these viral antigens to T cells, activating them. Once T cells are activated, T cells undergo clonal expansion, rapidly increasing their numbers (Griffin, 2016). They also differentiate into effector T cells, which are specialized to combat the virus. Two main types of T cells involved in the immune response against MV are CD4⁺ T helper cells and CD8⁺ cytotoxic T cells (Amanna and Slifka, 2011).

Helper T cells (CD4⁺ T cells)

It plays a central role in orchestrating the immune response by secreting cytokines that activate other immune cells. They help in the activation and differentiation of B cells, which produce antibodies against the virus. Additionally, CD4⁺ T cells provide help to CD8⁺ T cells, enhancing their cytotoxic activity (Griffin, 2016).

Cytotoxic T cells (CD8⁺ T cells)

It directly kills virus-infected cells by recognizing and destroying them. They recognize viral antigens presented on the surface of infected cells and release cytotoxic molecules such as perforin and granzymes to induce apoptosis (cell death) in the infected cells (Griffin, 2016; Uddbäck et al., 2024). CD8⁺ T cells can kill infected cells and help clear the infection. Following the resolution of the infection, a pool of memory T cells is formed. These cells provide long-term immunity against future encounters with the MV. Memory T cells can rapidly mount an immune response upon re-exposure to the virus, preventing or significantly reducing the severity of reinfection (Uddbäck et al., 2024). Overall, T cell-mediated immunity plays a crucial role in controlling MV infection, both by directly killing infected cells and by coordinating other components of the immune system. This multifaceted immune response is essential for effectively clearing the virus and providing long-term protection against measles.

B cells and antibody production

Humoral immunity is mainly mediated by antibodies produced by B cells that play a crucial role in the clearance of MV infection (Amanna and Slifka, 2010). Upon exposure to the MV, B cells are activated and undergo clonal expansion. Some of these B cells differentiate into plasma cells, which are specialized to produce antibodies specific to the MV antigens, these antibodies can neutralize the virus by binding to these surface proteins, preventing the virus from entering and infecting host cells (Mina et al., 2015; Amurri et al., 2022).

Following measles infection, a pool of memory B cells is formed. These cells have the ability to rapidly differentiate into plasma cells upon re-exposure to the MV, leading to a faster and more robust antibody response. The production of measles-specific antibodies, including immunoglobulin mega (IgM) and immunoglobulin gamma (IgG), are key aspects of the humoral immune response to MV infection and result in long-term immunity against measles (Amurri et al., 2022). IgM antibodies are the first type of antibodies produced in response to a new infection. IgM antibodies are typically detectable in the blood within a few days to weeks after the onset of symptoms and are indicative of recent or acute infection (Amanna and Slifka, 2011; Pérez Olmeda et al., 2022). In contrast to IgM, IgG antibodies are produced later in the course of infection and persist for a longer duration, providing long-term immunity against measles. As the immune response progresses, B cells undergo class switching, leading to the production of IgG antibodies specific to MV antigens. IgG antibodies play a crucial role in providing protection against reinfection by the MV. They can neutralize the virus, facilitate opsonization and phagocytosis, and activate the complement system (Amanna and Slifka, 2011; Pérez Olmeda et al., 2022). Detection of measles-specific IgM and IgG antibodies is commonly used for laboratory diagnosis of measles infection. IgM antibodies are particularly useful for diagnosing recent and acute infections, while IgG antibodies indicate past infection or immunity due to vaccination (Hübschen et al., 2017). The presence of measles-specific antibodies, especially IgG antibodies, is a crucial component of immunity against measles and is a primary goal of measles vaccination programs to achieve herd immunity and prevent outbreaks.

Formation of immunological memory

The formation of immunological memory to MV is a crucial aspect of long-term immunity against the virus. Immunological memory refers to the ability of the immune system to remember a previous encounter with a specific pathogen and mount a rapid and robust immune response upon re-exposure to the MV (Amurri et al., 2022). The presence of memory T and memory B cells provides long-term protection against MV infection (Amanna and Slifka, 2011). If an individual is re-exposed to the virus, either through natural infection or exposure to the measles vaccine, memory T and memory B cells rapidly recognize the virus and initiate a fast and robust immune response. This secondary immune response is typically faster and more effective than the primary response, leading to rapid clearance of the virus and prevention of severe disease (Mina et al., 2019). Taken together, the formation of immunological memory is essential for long-term immunity against MV and plays a critical role in preventing reinfection and maintaining population-level immunity.

Immune responses in measles complications

Immune amnesia following measles infection refers to the phenomenon where the MV causes a significant decrease in the body’s immune memory. This occurs because the virus infects and destroys immune cells that have previously encountered and remembered other pathogens (such as viruses and bacteria), leading to a weakened immune response against those pathogens (Mina et al., 2015). MV primarily targets and infects memory T cells, which are crucial for maintaining immunity against previously encountered pathogens. This infection results in the depletion of these memory T cells. Furthermore, with fewer memory T cells, the body loses its ability to mount a robust immune response upon re-exposure to pathogens it had previously encountered or been vaccinated against. This effect can last for months to years after the acute measles infection (Petrova et al., 2019). Taken together, this increased susceptibility for individuals who have experienced measles, potentially leading to increased illness and mortality from other infectious diseases. In addition to that, measles-induced immune amnesia can also impair the effectiveness of vaccines received prior to measles infection, reducing the protection provided by vaccines such as those against measles itself, as well as other diseases.

Regarding measles complications, MV can cause complications, such as pneumonia, encephalitis, and subacute sclerosing panencephalitis (SSPE) (Yentür et al., 2021), and immune responses play a complex role (Bellini et al., 2005). While the immune system’s response is intended to control and clear the MV, it can also contribute to tissue damage in some cases. Overall, while immune responses are essential for controlling MV infection, they can also contribute to tissue damage and pathology in measles complications such as pneumonia, encephalitis, and SSPE (Coughlin et al., 2013; Mina et al., 2015; Petrova et al., 2019). Understanding the complex interplay between the virus and the host immune system is crucial for developing effective treatments and interventions to prevent and manage these severe complications of measles.

Measles vaccination overview

The World Health Organization provides strategies aimed to achieve high vaccination coverage and prevent outbreaks and maintain herd immunity for vaccine-preventable diseases such as measles. Taken together, a combination of routine immunization, mass vaccination campaigns, catch-up vaccination, routine second-dose vaccination, and supplementary immunization activities is essential for achieving and sustaining high vaccination coverage and preventing measles transmission. These vaccination strategies are key components of measles control and elimination efforts worldwide (Minta et al., 2023).

Importance of herd immunity

Herd immunity, also known as community immunity, is critical for protecting populations from infectious diseases, especially those that are highly contagious like measles (Anderson and May, 1985; Fine et al., 2011).

Overall, herd immunity is a crucial public health concept that highlights the importance of vaccination and population-level immunity in preventing the spread of infectious diseases and protecting vulnerable individuals. By working together to achieve high vaccination coverage, communities can create a protective shield that benefits everyone, from the youngest and most vulnerable to the entire population. Measles elimination requires a comprehensive approach that addresses vaccine coverage, vaccine hesitancy, surveillance, outbreak response, and global collaboration. By implementing evidence-based strategies and building resilient immunization systems, countries can work towards the goal of measles elimination and protect populations from this highly contagious disease.

---

Conclusion

This review has highlighted the intricate interplay between MV and the human immune system. Insights into the dynamics of innate and adaptive immune responses have provided valuable knowledge for both understanding measles pathogenesis and informing vaccine development efforts.

In the era of emerging infectious diseases and global health challenges, a deeper understanding of human immune responses to measles is crucial for developing effective control measures and safeguarding public health. By leveraging advances in immunology, virology, and epidemiology, we can strive towards the ultimate goal of measles elimination and ensure a healthier future for generations to come.

---

Acknowledgments

None.

Conflict of interest

The author declares that there is no conflict of interest.

Funding

None.

Authors’ contributions

There is one author for this review article.

Data availability

All data are provided in the manuscript.

---

References

Abt, M., Gassert, E. and Schneider-Schaulies, S. 2009. Measles virus modulates chemokine release and chemotactic responses of dendritic cells. J. Gen. Virol. 90, 909–914. Available via https://doi.org/10.1099/vir.0.008581-0

Allen, I.V., McQuaid, S., Penalva, R., Ludlow, M., Duprex, W.P. and Rima, B.K. 2018. Macrophages and dendritic cells are the predominant cells infected in measles in humans. mSphere 3, e00570–17. Available via https://doi.org/10.1128/mSphere.00570-17

Amanna, I.J. and Slifka, M.K. 2011. Contributions of humoral and cellular immunity to vaccine-induced protection in humans. Virology 411, 206–215. Available via https://doi.org/10.1016/j.virol.2010.12.016

Amanna, I.J. and Slifka, M.K. 2010. Mechanisms that determine plasma cell lifespan and the duration of humoral immunity. Immunol. Rev. 236, 125–138. Available via https://doi.org/10.1111/j.1600-065X.2010.00912.x

Amurri, L., Reynard, O., Gerlier, D., Horvat, B. and Iampietro, M. 2022. Measles virus-induced host immunity and mechanisms of viral evasion. Viruses 14, 2641. Available via https://doi.org/10.3390/v14122641

Anderson, R.M. and May, R.M. 1985. Vaccination and herd immunity to infectious diseases. Nature 318, 323–329. Available via https://doi.org/10.1038/318323a0

Bellini, W.J., Rota, J.S., Lowe, L.E., Katz, R.S., Dyken, P.R., Zaki, S.R., Shieh, W.J. and Rota, P.A. 2005. Subacute sclerosing panencephalitis: more cases of this fatal disease are prevented by measles immunization than was previously recognized. J. Infect. Dis. 192, 1686–1693. Available via https://doi.org/10.1086/497169

Bellini, W.J., Rota, J.S. and Rota, P.A. 1994. Virology of measles virus. J. Infect. Dis. 170 Suppl 1, S15–23. Available via https://doi.org/10.1093/infdis/170.supplement_1.s15

Caligiuri, M.A. 2008. Human natural killer cells. Blood 112, 461–469. Available via https://doi.org/10.1182/blood-2007-09-077438

Clifford, H.D., Yerkovich, S.T., Khoo, S.K., Zhang, G., Upham, J., Le Souëf, P.N., Richmond, P. and Hayden, C.M. 2012. Toll-like receptor 7 and 8 polymorphisms: associations with functional effects and cellular and antibody responses to measles virus and vaccine. Immunogenetics 64, 219–228. Available via https://doi.org/10.1007/s00251-011-0574-0

Coughlin, M.M., Bellini, W.J. and Rota, P.A. 2013. Contribution of dendritic cells to measles virus induced immunosuppression. Rev. Med. Virol. 23, 126–138. https://doi.org/10.1002/rmv.1735

de Vries, R.D., Duprex, W.P. and de Swart, R.L. 2015. Morbillivirus infections: an introduction. Viruses 7, 699–706. Available via https://doi.org/10.3390/v7020699

de Vries, R.D., McQuaid, S., van Amerongen, G., Yüksel, S., Verburgh, R.J., Osterhaus, A.D.M.E., Duprex, W.P. and de Swart, R.L. 2012. Measles immune suppression: lessons from the macaque model. PLoS Pathog. 8, e1002885. Available via https://doi.org/10.1371/journal.ppat.1002885

Fine, P., Eames, K. and Heymann, D.L. 2011. “Herd immunity”: a rough guide. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 52, 911–916. Available via https://doi.org/10.1093/cid/cir007

Gerlier, D. and Valentin, H. 2009. Measles virus interaction with host cells and impact on innate immunity. Curr. Top. Microbiol. Immunol. 329, 163–191. Available via https://doi.org/10.1007/978-3-540-70523-9_8

Gerriets, V.A., Kishton, R.J., Johnson, M.O., Cohen, S., Siska, P.J., Nichols, A.G., Warmoes, M.O., de Cubas, A.A., MacIver, N.J., Locasale, J.W., Turka, L.A., Wells, A.D. and Rathmell, J.C. 2016. Foxp3 and toll-like receptor signaling balance treg cell anabolic metabolism for suppression. Nat. Immunol. 17, 1459–1466. Available via https://doi.org/10.1038/ni.3577

Griffin, D.E. 2016. The immune response in measles: virus control, clearance and protective immunity. Viruses 8, 282. Available via https://doi.org/10.3390/v8100282

Griffin, D.E. 2010. Measles virus-induced suppression of immune responses. Immunol. Rev. 236, 176–189. Available via https://doi.org/10.1111/j.1600-065X.2010.00925.x

Griffin, D.E., Ward, B.J., Jauregui, E., Johnson, R.T. and Vaisberg, A. 1990. Natural killer cell activity during measles. Clin. Exp. Immunol. 81, 218–224. Available via https://doi.org/10.1111/j.1365-2249.1990.tb03321.x

Hübschen, J.M., Bork, S.M., Brown, K.E., Mankertz, A., Santibanez, S., Ben Mamou, M., Mulders, M.N. and Muller, C.P. 2017. Challenges of measles and rubella laboratory diagnostic in the era of elimination. Clin. Microbiol. Infect. Off. Publ. Eur. Soc. Clin. Microbiol. Infect. Dis. 23, 511–515. Available via https://doi.org/10.1016/j.cmi.2017.04.009

Hübschen, J.M., Gouandjika-Vasilache, I. and Dina, J. 2022. Measles. Lancet Lond. Engl. 399, 678–690. Available via https://doi.org/10.1016/S0140-6736(21)02004-3

Jain, R. and Aulakh, R. 2022. Measles-associated CNS complications: a review. J. Child Sci. 12, e172–e181. Available via https://doi.org/10.1055/s-0042-1757914

Karp, C.L. 1999. Measles: immunosuppression, interleukin-12, and complement receptors. Immunol. Rev. 168, 91–101. Available via https://doi.org/10.1111/j.1600-065x.1999.tb01285.x

Kawai, T. and Akira, S. 2010. The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors. Nat. Immunol. 11, 373–384. Available via https://doi.org/10.1038/ni.1863

Koyama, S., Ishii, K.J., Coban, C. and Akira, S. 2008. Innate immune response to viral infection. Cytokine 43, 336–341. Available via https://doi.org/10.1016/j.cyto.2008.07.009

Laksono, B.M., de Vries, R.D., McQuaid, S., Duprex, W.P. and de Swart, R.L. 2016. Measles virus host invasion and pathogenesis. Viruses 8, 210. Available via https://doi.org/10.3390/v8080210

Lemon, K., de Vries, R.D., Mesman, A.W., McQuaid, S., van Amerongen, G., Yüksel, S., Ludlow, M., Rennick, L.J., Kuiken, T., Rima, B.K., Geijtenbeek, T.B.H., Osterhaus, A.D.M.E., Duprex, W.P. and de Swart, R.L. 2011. Early target cells of measles virus after aerosol infection of non-human primates. PLoS Pathog. 7, e1001263. Available via https://doi.org/10.1371/journal.ppat.1001263

Lin, L.T. and Richardson, C.D. 2016. The host cell receptors for measles virus and their interaction with the viral hemagglutinin (H) Protein. Viruses 8, 250. Available via https://doi.org/10.3390/v8090250

Mina, M.J., Kula, T., Leng, Y., Li, M., de Vries, R.D., Knip, M., Siljander, H., Rewers, M., Choy, D.F., Wilson, M.S., Larman, H.B., Nelson, A.N., Griffin, D.E., de Swart, R.L. and Elledge, S.J. 2019. Measles virus infection diminishes preexisting antibodies that offer protection from other pathogens. Science 366, 599–606. Available via https://doi.org/10.1126/science.aay6485

Mina, M.J., Metcalf, C.J.E., de Swart, R.L., Osterhaus, A.D.M.E. and Grenfell, B.T. 2015. Long-term measles-induced immunomodulation increases overall childhood infectious disease mortality. Science 348, 694–699. Available via https://doi.org/10.1126/science.aaa3662

Minta, A.A., Ferrari, M., Antoni, S., Portnoy, A., Sbarra, A., Lambert, B., Hatcher, C., Hsu, C.H., Ho, L.L., Steulet, C., Gacic-Dobo, M., Rota, P.A., Mulders, M.N., Bose, A.S., Caro, W.P., O’Connor, P. and Crowcroft, N.S. 2023. Progress toward measles elimination—Worldwide, 2000-2022. MMWR Morb. Mortal. Wkly. Rep. 72, 1262–1268. Available via https://doi.org/10.15585/mmwr.mm7246a3

Naniche, D. 2009. Human immunology of measles virus infection. Curr. Top. Microbiol. Immunol. 330, 151–171. Available via https://doi.org/10.1007/978-3-540-70617-5_8

Pérez Olmeda, M., Balfagón, P., Camacho, J., Dafouz, D., de la Fuente, J., Murillo, M.Á., Muñoz, J.L., Fernández García, A., Sanz, J.C. and de Ory, F. 2022. Comparative evaluation of assays for IgM detection of rubella and measles infections. Enfermedades Infecc. Microbiol. Clin. Engl. Ed 40, 22–27. Available via https://doi.org/10.1016/j.eimce.2020.06.020

Petrova, V.N., Sawatsky, B., Han, A.X., Laksono, B.M., Walz, L., Parker, E., Pieper, K., Anderson, C.A., de Vries, R.D., Lanzavecchia, A., Kellam, P., von Messling, V., de Swart, R.L. and Russell, C.A. 2019. Incomplete genetic reconstitution of B cell pools contributes to prolonged immunosuppression after measles. Sci. Immunol. 4, eaay6125. Available via https://doi.org/10.1126/sciimmunol.aay6125

Porter, A. and Goldfarb, J. 2019. Measles: a dangerous vaccine-preventable disease returns. Cleve. Clin. J. Med. 86, 393–398. Available via https://doi.org/10.3949/ccjm.86a.19065

Rota, P.A., Featherstone, D.A. and Bellini, W.J. 2009. Molecular epidemiology of measles virus. Curr. Top. Microbiol. Immunol. 330, 129–150. Available via https://doi.org/10.1007/978-3-540-70617-5_7

Tatsuo, H., Ono, N., Tanaka, K. and Yanagi, Y. 2000. SLAM (CDw150) is a cellular receptor for measles virus. Nature 406, 893–897. Available via https://doi.org/10.1038/35022579

Uddbäck, I., Michalets, S.E., Saha, A., Mattingly, C., Kost, K.N., Williams, M.E., Lawrence, L.A., Hicks, S.L., Lowen, A.C., Ahmed, H., Thomsen, A.R., Russell, C.J., Scharer, C.D., Boss, J.M., Koelle, K., Antia, R., Christensen, J.P. and Kohlmeier, J.E. 2024. Prevention of respiratory virus transmission by resident memory CD8+ T cells. Nature 626, 392–400. Available via https://doi.org/10.1038/s41586-023-06937-1

Wang, J.P., Kurt-Jones, E.A. and Finberg, R.W. 2007. Innate immunity to respiratory viruses. Cell. Microbiol. 9, 1641–1646. Available via https://doi.org/10.1111/j.1462-5822.2007.00961.x

Yentür, S.P., Demirbilek, V., Gurses, C., Baris, S., Kuru, U., Ayta, S., Yapici, Z., Adin-Cinar, S., Uysal, S., Celik Yilmaz, G., Onal, E., Cokar, O. and Saruhan-Direskeneli, G. 2021. Immune alterations in subacute sclerosing panencephalitis reflect an incompetent response to eliminate the measles virus. PloS One 16, e0245077. Available via https://doi.org/10.1371/journal.pone.0245077

Zhou, R., Liu, L. and Wang, Y. 2021. Viral proteins recognized by different TLRs. J. Med. Virol. 93, 6116–6123. Available via https://doi.org/10.1002/jmv.27265