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5
The Association Between Human
Cytomegalovirus and Neurocognitive
Disorders and Dementia
Guy D. Eslick
Introduction
Human cytomegalovirus (HCMV), also known as human betaherpesvirus 5, is a
member of the Herpesviridae family of viruses (Dioverti & Razonable, 2016). It is
one of the largest viruses known to cause infection with a viral particle diameter
of approximately 150– 200 nm (Schottstedt et al., 2010). It is an extremely common
infection worldwide with studies estimating seroprevalence rates close to 100 percent for Africa and Asia and lower at 50 percent in North America and 80 percent in
Europe (Al Mana et al., 2019; Cannon et al., 2010). HCMV is responsible for a wide
variety of clinical syndromes, which range from asymptomatic infection in healthy
individuals, to severe and potentially fatal disease in immunocompromised individuals (e.g., human immunodeciency virus patients, organ transplant recipients)
(Lancini et al., 2014; Stewart & Kotton, 2024).
Transmission of human cytomegalovirus
Pathways of transmission
e transmission pathways for HCMV are varied and are dependent on the age of acquisition. HCMV can aect any age group with transmission occurring in the following ways:
• Blood transfusion (Njeru et al., 2009)
• Organ transplantation (Silva Junior et al., 2023)
• Sexual activity (Handseld et al., 1985)
• Breastfeeding (Hu et al., 2021)
• Direct contact with urine (Delforge et al., 2017)
• Direct contact with saliva (Mayer et al., 2020)
Guy D. Eslick,
Neurocognitive and Neuropsychiatric Medicine
© Oxford University Press 2024. DOI: 10.1093/ oso/ 9780192870414.003.0006
Infectious Disease and Neurocognition
In vitro productive infection
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SVZ
BBB
BBB
CNS
In vivo infection
No information on
CMV latency
In vivo infection
In vitro productive infection
Possible site of CMV latency
Ependymal cell Microglia
2b 2a
2 CNS entry
3 Infection of brain cells
In vivo infection
In vitro productive infection
No information on
CMV latency
1 Migration
No information for in vivo infection
In vitro productive infection
No information on
CMV latency
OligodendrocyteMyeloid cellPericyte
CSF
SVZ
In vivo infection
In vitro productive infectio
Possible site of CMV latenc
NSPCsAstrocyte
CMVNeuron
Figure 5.1 Cytomegalovirus (CMV) infection in developing brain. CMV dissemination to the
central nervous system (CNS) is secondary to peripheral organ infection (1). Upon reaching the
brain, CMV is hypothesized to cross the blood– brain barrier (BBB) by either cell- associated (2a)
or cell- free form (2b). Monocytes are proposed to mediate cell- associated passage across the
BBB. Upon crossing of the BBB, CMV infects resident cells (3). Apart from oligodendrocytes, CMV
infection of resident CNS cells was confirmed in vivo. CMV DNA was detected in cerebrospinal
fluid (CSF) of congenitally infected infants and neural stem precursor cells (NSPCs), abundant in
subventricular zones (SVZ), are a prominent target of CMV infection.
Source: Created with BioRender.com. Krstanović, F., Britt, W. J., Jonjic, S. & Brizic, I. 2021. Cytomegalovirus
infection and inflammation in developing brain. Viruses, 13, 1078. https:// doi.org/ 10.3390/ v13061 078, https://
crea tive comm ons.org/ licen ses/ by/ 4.0/
• Direct contact with tears (Cox et al., 1975)
• Direct contact with semen (Lupton et al., 2014)
• Vertical transmission during childbirth (Pass & Anderson, 2014).
e process of HCMV infection is complex and will not be discussed in detail in this
chapter, but please see Figure 5.1 for a summary of the process.
Viral latency
A major issue with HCMV is that it leads to lifelong infection associated with latency; the virus can reactivate at any time, and this is especially critical for those who
Cytomegalovirus 65
are immunocompromised or undergoing organ transplantation (Schwartz & SternGinossar, 2023). Moreover, the exact mechanism by which latency occurs is not
completely understood (Goodrum, 2022). Please see Figure 5.2 for a comparison of
acute and latent infection. is is an evolving eld of research for all latent viruses
that impact humans (Crawford et al., 2022; O’Connor, 2021; Smith et al., 2021).
Figure 5.2 Immune response to cytomegalovirus (CMV) infection in the brain. (a) Acute
infection. Upon crossing of the blood– brain barrier (BBB), CMV infects resident cells (1).
Astrocyte- derived chemokines recruit microglia to the infection site (2a). Microglia are
activated via pattern recognition receptors and cytokines. Activated microglia produce
proinflammatory cytokines (2b), which mediate immune cell recruitment into the brain (3) and
orchestrate immune cell response (4). Infiltrating NK cells and ILC1 cells produce interferon
gamma (IFN- γ) and myeloid cells produce tumor necrosis factor alpha (TNF- α), leading to
organ- wide polarization of microglia (5); infiltrating T cells provide direct control of productive
infection (6). CD8+ and CD4+ T cells recognize virus- infected cells in the context of major
histocompatibility complex (MHC) I and MHC II molecules and provide virus control by cytolytic
mechanisms (gzmB) or by non- cytolytic mechanisms (IFN- γ). (b) Latent infection. Following
resolution of acute CMV infection, T cells are retained in the brain as tissue- resident cells (TRM)
and control latent/ reactivating CMV. CD8+ TRM cells are characterized by expression of CD69
and integrin CD103, while CD4+ TRM cells express CD69 and CD11a. Both cytolytic mechanisms
(gzmB) and cytokines (IFN- γ) could mediate the control of latent and reactivating CMV in the
CNS. TRM cells are suggested to persist in the brain of mice for a lifetime without or with minimal
replenishment from the circulation. Activated microglia probably contribute to maintenance
and functional capacity of TRM cells in the brain.
Source: Created with BioRender.com. Krstanović, F., Britt, W. J., Jonjic, S. & Brizic, I. 2021.
Cytomegalovirus infection and inflammation in developing brain. Viruses, 13, 1078. https:// doi.
org/ 10.3390/ v13061 078, https:// crea tive comm ons.org/ licen ses/ by/ 4.0/
Infectious Disease and Neurocognition
Congenital transmission
Transplacental transmission (congenital CMV (cCMV)) is an extremely important
mode of disease transmission in humans (Caneld et al., 2023; Pass & Anderson,
2014). e reason for this is that mother- to- child transmission of the virus provides a method of transmission that maintains a cycle of infection within the human
species. Currently, there are no eective prenatal or antenatal preventive strategies (Caneld et al., 2023). Unfortunately, because of this, there are no universal
screening approaches being oered. Suspected cases of cCMV should have a histopathological assessment of the placenta to identify CMV viral particles (Figure 5.3).
For postnatal diagnosis, the development of a potential vaccine is ongoing, but no
phase III clinical trials have been conducted.
Congenital CMV is a rare condition, but it is the most common congenital infection in developed countries (Krstanović et al., 2021). In Australia, the Australian
Paediatric Surveillance Unit (APSU) conducts annual national surveillance on
cCMV; the study has been running for 24 years and is the longest study on cCMV
in the world (Teutsch et al., 2023). For example, the annual surveillance for 2022 reported 33 conrmed cases; this equates to an annual incidence of 11.15/ 100,000 live
births (95 percent condence interval (CI): 7.93– 15.68) or approximately 300,000
births annually in Australia (Krstanović et al., 2021).
Neurocognitive and neuropsychiatric function
Pediatric population
Studies suggest that clinical disease associated with cCMV occurs in up to 15 percent of newborns (Jones et al., 2023). e severity of clinical disease ranges from
mild to severe, and neurological abnormalities only represent one component of the
possible problems related to cCMV infection, with other problems including rash,
hepatosplenomegaly, and chorioretinitis.
Figure 5.3 Photomicrograph showing cytomegalovirus intranuclear inclusions (arrows) in
villous stromal cells (×400 magnification).
Source: Canfield, D., Gabby, L., Vaziri Fard, E. & Gyamfi- Bannerman, C. 2023. Cytomegalovirus in pregnancy.
Obstet Gynecol Clin North Am, 50, 263– 277. Reprinted with permission from Elsevier.
Cytomegalovirus 67
Hearing loss
An important clinical problem associated with cCMV infection in newborns is sensorineural hearing loss (SNHL), which may be the only neurological decit due to
cCMV infection (Engman et al., 2008). A 2023 prospective study compared 40 children aged 6– 7 years with cCMV to 54 healthy cCMV- negative controls matched for
sex, gestational age, date of birth, and neonatal ward (Kokkola et al., 2023). All children were assessed using pure- tone audiometry, and the denition of hearing loss
was a pure- tone average greater than 20 dB. Other assessments included vestibular
function, which measures the function of the semicircular canal via the video head
impulse test (Kokkola et al., 2023). e study reported that children with cCMV had
higher rates of vestibular dysfunction compared to healthy controls (19.4 percent
versus 3.2 percent, p = 0.06), although this was not statistically signicant. Moreover,
rates of SNHL were higher in children with cCMV compared to controls (10.5 percent versus 0 percent, p = 0.12), although again this was not statistically signicant.
Of note, all cases of hearing loss were unilateral. is study highlighted that vestibular dysfunction may be more common than SNHL at 6 years of age and that vestibular tests should be included in all hearing assessments of children with cCMV
(Kokkola et al., 2023).
Cognitive function
A case– control study assessing long- term neuropsychological complications among
very preterm children with cCMV (n = 19/ 42) compared with term- born controls (n = 24) found dierences in cognitive function (Brecht et al., 2015). ose
in the preterm group were between ages 11.6 and 16.2 years (mean: 13.9 years) and
36 percent were female, compared to the term controls who were aged between 11.3
and 16.6 years (mean: 13.6 years) and 50 percent were female. Children were assessed using the Wechsler Intelligence Scale and the Developmental Test for Visual
Perception. e analysis found that adolescents who were born preterm with cCMV
had lower scores on the cognitive test compared to controls (92.67 versus 102.75,
p = 0.03) (Figure 5.4). However, there was no statistically signicant dierence in
scores for visuoperceptive abilities between those with cCMV and controls (91.22
versus 98.96, p > 0.05). In addition, a post hoc analysis identied sex dierences for
IQ among those who were cCMV- positive and cCMV- negative with males having
lower scores (Brecht et al., 2015). Overall, these ndings suggest that cCMV appears to be a factor associated with cognitive abilities during adolescence; however,
it should be noted that this study did not adjust for other potential confounding factors that might account for such IQ scores and that the relatively small sample size
might explain why some analyses did not reach statistical signicance.
A recent study conducted on a sample of adolescents aimed to assess the interplay between latent HCMV infection, schizophrenia spectrum disorder, and the
impact on cognitive function assessed via the intelligent quotient (IQ) (Calkova
et al., 2022). All 17 adolescent patients had schizophrenia spectrum disorders (mean
age: 16.7 years, 71 percent female), with approximately one- third (31 percent)