Acquired immunodeficiency syndrome-associated cytomegalovirus encephalitis: clinical, imaging, and follow-up characteristics of 11 cases

Introduction

Acquired immunodeficiency syndrome (AIDS) is a chronic infectious disease caused by the human immunodeficiency virus (HIV). HIV primarily targets the host immune system, causing a progressive decline in CD4⁺ T-lymphocyte counts and leading to severe cellular immunodeficiency, which predisposes patients to a wide range of opportunistic infections and neoplasms (1). Cytomegalovirus (CMV) infection is among the most prevalent opportunistic complications in individuals with AIDS (2).

CMV is a double-stranded deoxyribonucleic acid (DNA) herpesvirus, also designated human herpesvirus 5 (HHV-5). It is primarily transmitted through saliva, blood, sexual contact, vertical mother-to-child transmission, and organ transplantation. After primary infection, the virus establishes lifelong latency within the monocyte–macrophage lineage and vascular endothelial cells, with potential reactivation when host immunity wanes (3). In immunocompromised hosts—such as individuals with HIV/AIDS or solid-organ transplant recipients—CMV reactivation frequently leads to viremia and dissemination to multiple organs (4).

Central nervous system involvement most commonly manifests as encephalitis or polyradiculitis (5), and is particularly prevalent in advanced AIDS. In cases of severe immunodeficiency (CD4⁺ T-lymphocyte count <50 cells/µL), CMV encephalitis can directly invade cerebral parenchyma and is associated with high mortality (6). Although combination antiretroviral therapy (ART) has markedly prolonged the survival of AIDS patients, the clinical presentation of CMV encephalitis remains non-specific, often resulting in delayed or missed diagnosis.

Due to its high spatial resolution and superior soft-tissue contrast, magnetic resonance imaging (MRI) plays a pivotal role in the early detection and characterization of CMV encephalitis (7). The current literature mainly comprises case reports and small cross-sectional studies; however, large-scale systematic analyses with longitudinal follow-up are lacking, limiting the comprehensive assessment of the diagnostic value of MRI. To address this gap in the literature, we conducted a retrospective analysis of the imaging findings in 11 AIDS patients with CMV encephalitis, evaluated their MRI characteristics, and performed extended clinical follow-up. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2399/rc).

Methods

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Ethics Committee of The Fourth People’s Hospital of Nanning {Nanning Talent Highland Project, No. [2023]01}. The requirement of informed consent was waived due to the retrospective nature of the study.

Study population

Clinical charts and cranial MRI examinations of 11 consecutive patients with AIDS-associated CMV encephalitis treated at The Fourth People’s Hospital of Nanning between April 2019 and August 2024 were retrospectively reviewed. The cohort comprised eight men and three women, aged 25–59 years (mean age: 45±13 years).

AIDS was diagnosed according to the 2024 Chinese national guidelines (8), with all patients demonstrating positive HIV antibody screening and confirmatory tests, in addition to compatible clinical manifestations. CMV encephalitis was defined by the presence of CMV DNA in cerebrospinal fluid (CSF) (8), detected by real-time polymerase chain reaction (PCR).

Immune reconstitution inflammatory syndrome (IRIS) is a potential complication in AIDS patients after ART, particularly during immune recovery, when excessive activation of the immune system can trigger an exacerbated inflammatory response (9).

Currently, there are no unified diagnostic criteria for CMV encephalitis-associated IRIS. Based on the diagnostic criteria for tuberculosis-associated IRIS (10), the key diagnostic features of CMV encephalitis-associated IRIS include: (I) a decrease in HIV RNA levels and/or a rapid increase in the CD4⁺ T-lymphocyte count after ART initiation; (II) new onset or worsening of neurological symptoms consistent with CMV encephalitis after ART; and (III) exclusion of alternative causes (e.g., new infections, drug resistance, adverse drug reactions, or relapse).

Imaging protocol

All examinations were performed on a 1.5-T Siemens Essenza scanner (Siemens Healthineers, Erlangen, Germany). The standardized protocol included axial T1-weighted imaging (T1WI) with sagittal sequences, T2-weighted imaging (T2WI), T2 fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) with b-values of 0 and 800 s/mm² following the standard brain DWI protocol at The Fourth People’s Hospital of Nanning. Post-contrast T1WI was obtained in axial, sagittal, and coronal planes after the intravenous administration of gadopentetate dimeglumine (18 mL) at an injection rate of 2.0 mL/s.

Image analysis

Digital images were uploaded to the institutional picture archiving and communication system (PACS) workstation and independently reviewed by two attending-level neuroradiologists. Discrepancies were resolved by consensus. For each lesion the following parameters were recorded: number (solitary vs. multiple), anatomical location, signal intensity on T1WI, T2WI/FLAIR, and DWI, apparent diffusion coefficient (ADC) values, and pattern of contrast enhancement.

Results

Clinical manifestations and laboratory findings

Of the 11 patients, 5 (45.5%) presented with neurological symptoms (headache, dizziness and dysarthria), 4 (36.4%) with intermittent or persistent fever, and 2 (18.2%) with visual loss. The median peripheral CD4⁺ T-cell count was 18 (interquartile range, 8–53) cells/µL (range, 2–257 cells/µL); and 8 patients (72.7%) had <50 cells/µL.

CSF CMV DNA was quantified by real-time PCR and ranged from 5.97×10² to 3.04×10⁴ copies/mL; concurrent CMV viraemia was documented in five patients. Among the 11 patients, 3 (27.3%) had detectable CMV immunoglobulin G (IgG) in CSF, whereas CMV immunoglobulin M (IgM) was uniformly negative. Detailed clinical data are summarized in Table 1.

MRI features

Lesions were solitary in 4 (36.4%) and multiple in 7 (63.6%) patients, yielding a total of 51 intracranial foci. In terms of distribution, there were 15 lesions in the cerebellum (29.4%), eight lesions in the frontal lobe (15.7%), five lesions each in the brainstem, basal ganglia, and ependyma (9.8% each), three lesions each in the occipital lobe, parietal lobe, thalamus, and corpus callosum (5.9% each), and one lesion in the insula (2.0%). In terms of the signal characteristics, on T1WI, the lesions were iso- and hypointense in 11 (21.6%) and 40 (78.4%) cases, respectively; on T2WI/FLAIR, the lesions were iso- and hyperintense in 5 (9.8%) and 46 (90.2%) cases, respectively; and on DWI, the lesions were hyperintense in 48 lesions (94.1%). The ADC values were low in 31 (60.8%) lesions, isointense in 8 (15.7%), and high in 8 (15.7%). Among the eight patients (33 lesions) who underwent contrast-enhanced MRI, 18 lesions (54.5%) showed no enhancement, while nodular and ring-like enhancements were observed in 6 (18.2%) and 9 (27.3%) lesions, respectively. Representative images are provided in Figures 1-4.

Figure 1 Solitary nodule in the left basal ganglia (a 28-year-old male) (arrows). (A) DWI shows hyperintensity. (B) ADC map shows central restricted diffusion with peripheral edema. (C) FLAIR shows hyperintensity. (D) Post-contrast T1WI shows nodular enhancement. ADC, apparent diffusion coefficient; DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery; T1WI, T1-weighted imaging.

Figure 2 Lesions located in the lateral ventricular walls and left basal ganglia (a 59-year-old female). (A,B) Hyperintense lesions along the walls of both lateral ventricles (thick arrow) and in the left basal ganglia (thin arrow) on DWI. (C,D) Corresponding hyperintensity in the same regions on T2WI. DWI, diffusion-weighted imaging; T2WI, T2-weighted imaging.

Figure 3 MRI evolution of intracranial lesions (a 25-year-old male). April 03, 2023: (A) hyperintense lesion in the right aspect of the genu of the corpus callosum (arrow) on DWI; (B) no enhancement on post-contrast scan. July 04, 2023: (C-E) original lesion had diminished in size; newly emerged hyperintense DWI foci were observed in the left hippocampus (arrow in C), left basal ganglia (arrow in D), and left aspect of the splenium of the corpus callosum (E, diagonal arrow). February 13, 2025: (F) no abnormal signal was observed within the brain parenchyma. DWI, diffusion-weighted imaging; MRI, magnetic resonance imaging.

Figure 4 The evolution of intracranial lesions during IRIS occurrence (a 58-year-old male). August 06, 2024: (A) hyperintense lesion in the left frontal lobe on DWI; (B) ring enhancement on post-contrast imaging. August 29, 2024: (C) DWI shows shrinkage of the left frontal lesion; (D) corresponding reduction in ring enhancement. Arrows indicate left frontal lobe. October 22, 2024: (E) further decrease in left frontal DWI hyperintensity, arrow indicates left frontal lobe; (F) post-contrast scan reveals increased and more extensive enhancement; a new enhancing nodule has appeared in the left parietal lobe (thick arrow); (G) the new parietal lesion (arrow) is hyperintense on DWI; (H) it demonstrates ring enhancement, arrow indicates the new parietal lesion. DWI, diffusion-weighted imaging; IRIS, immune reconstitution inflammatory syndrome.

Follow-up and outcome

Of the 11 patients, eight received combination therapy with ganciclovir plus foscarnet, and three received ganciclovir alone. At discharge, eight patients showed improvement, one was discharged against medical advice, and two died. During the 4-year post-discharge follow-up, five patients were lost, and four developed IRIS. The comparison of CD4⁺ T-lymphocyte counts between pre-ART and IRIS onset is presented in Table S1.

The MRI findings of IRIS in these four cases were compared with the pre-ART MRI findings, and the lesion changes were as follows:

• Case 1: partial regression of original lesions (with decreased DWI signal) and partial enlargement, with new lesions appearing (showing high DWI signal and ring enhancement);
• Case 2: regression of original lesions, with new lesions appearing (showing high DWI signal without enhancement);
• Case 3: regression of original lesions (with surrounding edema reduction), with new lesions appearing (showing high DWI signal and ring enhancement);
• Case 4: regression of original lesions (with decreased DWI signal and aggravated surrounding edema).

Discussion

AIDS patients with profound immunosuppression frequently fail to mount a detectable humoral response to CMV. Consistent with Zhao et al. (11), none of our patients had a positive CMV-IgM antibody. Eight individuals had peripheral CD4⁺ T-lymphocyte counts <50 cells/µL, confirming that advanced AIDS is a major risk factor for intracerebral CMV infection (12). Serial monitoring of CD4⁺ T-lymphocyte counts is thus essential for the early detection and preemptive management of HIV-related opportunistic infections (13). It should be noted that in advanced AIDS patients presenting with central nervous system symptoms, even negative blood CMV PCR and negative CMV-IgG test results cannot completely exclude the possibility of CMV encephalitis. Thus, MRI is critical for the early diagnosis of CMV encephalitis complicating AIDS.

Hyperintensity on T2WI and FLAIR images reflects vasogenic edema, active inflammation, and viral infiltration of brain parenchyma (14). In our series, eight lesions abutted the ependyma or lined the ventricular wall, all appearing hyperintense on DWI. Owing to its neurotropic predilection for ventricular surfaces (15), CMV typically produces ventriculitis or ependymitis that begins in the subependymal zones (16). Consequently, linear or patchy DWI hyperintensity along the ventricular margin is considered a highly specific early indicator of CMV infection (17).

Among the eight patients who underwent contrast-enhanced imaging, 33 lesions were identified: 18 showed no enhancement, six exhibited nodular enhancement, and nine displayed ring enhancement. Gadolinium leakage on post-contrast MRI indicates focal blood-brain barrier (BBB) disruption, but may also reflect perivascular inflammation, reactive gliosis, or increased vascular permeability (17,18). The degree of enhancement is therefore closely related to local perfusion and the integrity of the BBB. Non-enhancing foci either retain an intact barrier or represent quiescent, low-activity disease. Conversely, nodular or ring enhancement likely reflects extensive parenchymal congestion and oedema, accompanied by plasma-cell and lymphocytic infiltration that damages endothelial cells and increases permeability, ultimately, breaking down the BBB (5); necrosis or granuloma formation may contribute (19). Inter-individual variability in immune reactivity to CMV (20) further modulates these patterns. Thus, divergent enhancement most likely reflects differences in pathophysiology, disease stage, and host response.

The MRI findings of CMV encephalitis should be differentiated from other conditions. For example, cerebral infarction typically follows vascular territories (e.g., basal ganglia and corona radiata), assumes a wedge-shaped configuration, and shows homogeneous DWI hyperintensity with markedly reduced ADC in the acute phase (21). While toxoplasma encephalitis has a predilection for the basal ganglia, thalamus, and corticomedullary junction (22,23), appearing as isointense or hypointense on T1WI and hyperintense on T2WI/FLAIR, with contrast-enhanced scans demonstrating multiple eccentric thick-walled ring enhancements. The “eccentric target sign” is a relatively specific marker, accompanied by perilesional vasogenic edema and mass effect disproportionate to the size of the lesions (22).

In one patient, imaging revealed a solitary nodule in the left basal ganglia (Figure 1). Notably, the patient tested negative for both toxoplasma IgG and IgM antibodies, did not receive empirical anti-toxoplasma therapy, and showed clinical improvement with anti-CMV treatment alone. All patients in our cohort underwent CSF toxoplasma IgG testing, with all results being negative.

Primary central nervous system lymphoma (PCNSL), a malignant B-cell lymphoma, grows rapidly and is commonly seen in immunocompromised patients. Lesions are often associated with high-density angiogenesis (24). Solitary lesions are more common, located in deep cerebral white matter, the corpus callosum, or periventricular regions. MRI shows isointense signals on T1WI and hypointense signals on T2WI. Obvious homogeneous enhancement is the most typical feature on enhanced scans, with clear lesion boundaries (25,26).

CMV encephalitis demonstrates variable enhancement patterns (no enhancement, nodular enhancement, or ring enhancement). Due to dense cellularity, PCNSL exhibits markedly restricted diffusion on DWI sequences, with significantly decreased ADC values, which is an important basis for distinguishing lymphoma from other lesions (26).

Cranial tuberculosis is a granulomatous lesion caused by Mycobacterium tuberculosis infection, characterized by central caseous necrosis with surrounding fibrosis (27). Intracranial tuberculosis often manifests as meningeal enhancement (particularly prominent at the skull base), accompanied by hydrocephalus. Tuberculomas typically present as multiple nodules of varying sizes, located both supratentorially and infratentorially, with obvious meningeal enhancement. On T2WI, tuberculomas show heterogeneous signals, with the central necrotic area appearing hyperintense, and the periphery showing an isointense or hypointense ring. Contrast-enhanced scans demonstrate ring enhancement (with relatively smooth walls) or nodular enhancement (28,29). Although this ring enhancement pattern is similar to the partial ring-enhancing lesions seen in CMV encephalitis, the basal cistern enhancement in tuberculous meningitis and the multifocal nature of tuberculomas are important distinguishing features.

The initiation of ART in AIDS patients with CMV encephalitis may precipitate CMV-related IRIS. Recovery of CMV-specific immunity can trigger an exaggerated inflammatory response to viral antigens, resulting in increased cerebral inflammation, oedema, and neurological dysfunction (30). In our cohort, four patients developed CMV-encephalitis-associated IRIS 2–12 weeks after ART initiation. All four showed regression of the original lesions; three also exhibited new foci that were hyperintense on DWI. Post-contrast imaging revealed no enhancement in one patient and ring enhancement in two patients.

Limitations

The relatively small sample size and the absence of large-scale external data limit the generalizability and robustness of our findings. In addition, diagnosis relied primarily on PCR detection rather than histopathological confirmation. Future work should therefore expand the cohort and adopt a multicentre design to validate these observations. An additional key limitation of this study is the lack of serial HIV viral load measurements for these four IRIS cases—follow-up HIV viral load testing was not performed during the period of neurological deterioration or at the time of new MRI lesion appearance. Without these data, we cannot definitively demonstrate that immune reconstitution had occurred at the time of clinical worsening. The diagnosis of IRIS in these cases was based on clinical and radiological criteria in the context of recent ART initiation, but could not be confirmed by virological evidence of immune reconstitution.

Conclusions

MRI offers excellent depiction of intracranial lesions in AIDS-associated CMV encephalitis and shows disease-specific features, including predominant hyperintensity on T2WI/FLAIR, diffusion restriction on DWI, a periventricular predilection, and absent, nodular, or ring enhancement after contrast. IRIS is an important complication after ART initiation, especially in patients with CD4⁺ T-lymphocyte counts <50 cells/µL. MRI serves not only as a diagnostic modality but also as a non-invasive tool for the longitudinal monitoring of therapeutic response.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2399/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2399/dss

Funding: This work was supported by the Scientific Research and Technology Development Projects of Xingning District (No. 2022A11).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2399/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the institutional ethics committee of The Fourth People’s Hospital of Nanning {Nanning Talent Highland Project, No. [2023]01}. Informed consent was waived in this retrospective study.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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