Rapidly Progressive and Relapsing Myelitis With Human T Lymphotropic Virus Type 1

Abstract

A patient presented to our center in the northeastern United States with recurrent longitudinally extensive myelitis which was ultimately attributed to infection with human T lymphotropic virus type 1 (HTLV-1). The most common neurologic presentation of this infection is an insidiously progressive myelopathy, although reports of rapid progression with acute onset have been described, including some associated with inflammatory changes on spinal cord MRI. Here, we describe a case of this rare entity and provide a review of the clinical, diagnostic, and treatment data of similar published cases. Along with our case, 44 published cases of rapidly progressive or relapsing HTLV-1–associated myelopathy (HAM) were identified and included in this review. Patients were predominantly female and from Japan, the Caribbean, or South America with a median time from clinical onset to presentation of 5 months. There were radiographic features of myelitis in 98% of patients, with 93% showing longitudinally extensive lesions and only 1 patient with normal spinal MRI. Most patients received steroid therapy and 94% of patients experienced symptomatic or radiographic improvement after treatment, although longitudinal follow-up of these patients was limited. In summary, HAM may present as a rapidly progressive or relapsing myelitis. Patients with acute myelitis should be tested for HTLV-1 infection, especially in cases of longitudinally extensive myelitis with relevant exposure risk factors and negative testing for alternate diagnoses. Although these patients often experience clinical and radiographic improvement with steroid therapy, further work is needed to clarify whether this treatment influences chronic disease progression.

Introduction

Human T lymphotropic virus type 1 (HTLV-1) is a human retrovirus endemic to southwestern Japan and the Caribbean basin as well as portions of South America, Africa, and West Asia^1-4 with cases rarely encountered in other parts of the world, including the mainland United States (U.S.).^5,6 While contemporary estimates suggest a prevalence of 5–10 million HTLV-1 infected individuals within endemic regions,^4,7,8 estimations of global prevalence have historically been limited by lack of dedicated population-based epidemiologic studies, incomplete and biased sampling (e.g., screening of healthy blood donors), HTLV-1 assay performance, and the heterogenous distribution of infection within endemic populations.^8-10

The virus is largely transmitted through breast feeding, transfusion of nonleukocyte depleted blood products, unprotected sexual intercourse, sharing of contaminated needles, and solid organ transplantation.^7,9,10 Most infected individuals are asymptomatic carriers, although an estimated 4%–9% of those infected will develop disease associated with HTLV-1 which primarily includes adult T-cell leukemia/lymphoma (2%–6%) and an insidiously progressive inflammatory myelopathy known as HTLV-1–associated myelopathy or tropical spastic paraparesis (HAM/TSP, 2%–3%).¹¹ A variety of systemic inflammatory syndromes have also been attributed to HTLV-1 infection, including dermatitis, uveitis, pneumonitis, arthritis, and myositis among others.^11-13

An acute myelitis with rapid progression is an unusual complication of HTLV-1¹⁴ and has been associated with longitudinally extensive signal abnormalities in the spinal cord on MRI.^15-17 This clinical-radiographic syndrome has not been incorporated into the most recently revised diagnostic classification for HAM/TSP¹⁴ and is likely underdiagnosed outside endemic regions with limited data available to guide management.¹⁸ Here, we describe a case report of a patient who presented to our center in the northeastern United States with this rare entity and provide a review of the clinical, diagnostic, and treatment data of similar published cases.

Methods

Written informed consent was obtained from the patient presented in our case history. To supplement the literature review, her data were pooled along with systematically collected clinical, diagnostic, and treatment data from published cases of rapidly progressive or relapsing myelitis associated with HTLV-1 that included spine imaging during diagnostic evaluation. These patients were identified through the following PubMed query: (“HTLV-I Infections” [MeSH Terms]) AND (“paraparesis, tropical spastic” [MeSH Terms] OR “myelitis, transverse” [MeSH Terms] OR “Myelitis” [MeSH Terms]) AND (“rapidly progressive” [All Fields] OR “subacute” [All Fields] OR “relapsing” [All Fields]). Additional cases were identified through citation review. Cases in whom complete spinal imaging was not performed or those with other active culprit infections (e.g., HTLV-2, HIV, syphilis) or neuroinflammatory conditions (e.g., seropositive neuromyelitis optica spectrum disease [NMOSD], myelin oligodendrocyte glycoprotein antibody-associated disease [MOGAD], or neurosarcoidosis) were excluded from analysis. The literature search was updated continuously through November 2025. Where possible, units of measurement were standardized across cases. A timeline of our patient's clinical course and flowchart of case selection is included (eFigures 1 and 2).

Case Presentation

A 47-year-old woman presented to our center in June 2024 with several weeks of subjective fevers, headache, truncal paraspinal cramping, and diffuse rash characterized by pruritic, erythematous macules in a nondermatomal pattern over her shoulders, back, and thighs. She had no recent travel and reported no antecedent infectious or environmental exposures. She was not encephalopathic and had no meningismus or neurologic deficits. She had been previously healthy apart from chronic radicular cervicalgia of the left arm with cervicogenic head pain after a whiplash injury for which she underwent anterior discectomy and fusion (C5-C6, C6-C7) years prior. There were no chronic medical problems in her family. She was born on the west coast of the United States and lived in Puerto Rico with her mother for several years as an adolescent, although since age 15 years had lived in the northeastern United States. Initial serum testing disclosed leukocytosis (16,300 cells/μL, 19% small, atypical lymphocytes with irregular nuclei, condensed chromatin, and scant cytoplasm) with elevated markers of inflammation, as well as positive West Nile virus IgG (negative IgM) and heterophile testing (Epstein-Barr virus PCR not performed). Spinal fluid analysis was notable for lymphocytosis (24 cells/μL, 70% atypical lymphocytes) with mildly elevated protein (57 mg/dL) and negative testing for herpes simplex, varicella, West Nile, and Lyme. She was given supportive care and discharged home with a diagnosis of aseptic meningitis from presumed infectious mononucleosis.

Over the following 3 months, her rash improved but her myalgias and cramping persisted with increasing intensity, and by September 2024, she had developed low back pain, intermittent tonic spasm of the trunk and legs, mild paraparesis, and gait instability with urinary and bowel retention. On neurologic examination, there was mild weakness of the left arm and both legs, diffusely brisk reflexes with bilateral Hoffman sign, and a spastic, mildly ataxic gait. Cranial MRI demonstrated normal brain parenchyma. Spinal MRI demonstrated diffuse cervical cord edema, as well as enhancing T2 prolongation which extended contiguously from the medullary pyramids through the conus medullaris and prominently involved the lateral columns (Figure 1A). Laboratory evaluation revealed persistent lymphocytosis in the CSF along with increased CSF protein and oligoclonal bands (9 total, Table 1). Serum cell-based assays for aquaporin 4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) IgG were negative. Flow cytometry from the serum and CSF was unremarkable. HTLV-1 antibodies were strongly positive in the serum (screening ELISA with confirmatory Western blot), but this test was not performed in CSF (Table 1). Paraneoplastic antibody panels (including amphiphysin, AGNA-1, ANNA-1, ANNA-2, ANNA-3, CRMP-5, DPPX, GABA-B, GAD-65, GFAP, mGluR1, neurochondrin, neuronal intermediate filament, PCA-1, PCA-2, septin-7, and TRIM46) from the serum and CSF were negative. Serum testing for systemic autoantibodies (including antinuclear, Sjögren, double stranded DNA, Smith, ribonucleoprotein, and antiphospholipid) was negative, and additional serum and CSF testing for various infectious, inflammatory, and metabolic disorders was unremarkable. Whole-body PET was unavailable, although there was no evidence of solid malignancy or granulomatous disease on contrast-enhanced CT imaging of the chest and abdomen. Skin biopsy showed nonspecific inflammatory changes with superficial fungal infection. She received 3 days of pulse IV methylprednisolone (IVMP, 1,000 mg daily) with significant improvement in her myalgias with some improvement in her weakness, although persistent neurogenic bladder and bowel requiring intermittent catheterization and laxatives. She was discharged home with physiotherapy, at which time the differential diagnosis included sarcoidosis, paraneoplasia, and other immune-mediated or indolent infectious myelitis.

Figure 1. Serial Spinal MRI for Case Report.

(A) September 2024 (3 months from initial onset, before steroid): Sagittal short tau inversion recovery (STIR) and contrast-enhanced T1-weighted (T1+C) MRI of the cervical spine (top panel) and thoracic spine (bottom panel) with adjacent T2-weighed (T2) and T1+C sequences in the axial plane. There is T2 prolongation within the medullary pyramids which extends contiguously through the lateral columns of the rostral cervical cord before transitioning to ill-defined signal transversely involving the entire cord from the lower cervical segments through the conus medullaris. This abnormal signal is associated with enhancement which extends contiguously from the medullary pyramids through the lateral columns of the cervical and thoracic cord. There is cord edema prominently involving the cervical segments and to a lesser degree the thoracic segments. (B) November 2024 (5 months from initial onset, 9 weeks after initial steroid, 4 weeks after second steroid): Sagittal STIR MRI of the cervical spine (top panel) and thoracic spine (bottom panel) with adjacent T2 and T1+C sequences in the axial plane. The cervical and thoracic cord edema has resolved. There is faint residual T2 prolongation within the medullary pyramids which extends longitudinally in a patchy fashion from the medullary pyramids through the lateral columns of the cervical and thoracic cord. There is no apparent abnormal enhancement within the cervical cord. There are faint, patchy foci of enhancement within the lateral columns of the thoracic cord. (C) July 2025 (13 months from initial onset, 6 weeks into second flare, before steroid): Sagittal STIR and T1+C MRI of the cervical spine (top panel) and thoracic spine (bottom panel) with adjacent T2 and T1+C sequences in the axial plane, including copies of the axial T1+C films with abnormal enhancement highlighted in yellow. There is recurrent cord edema most prominently involving the cervical segments. There is worsening T2 prolongation within the medullary pyramids which extends contiguously through the lateral columns of the rostral cervical cord before transitioning to ill-defined signal transversely involving the entire cord from the rostral cervical segments through the conus medullaris. This abnormal signal is again associated with enhancement which extends contiguously from the medullary pyramids through the lateral columns of the cervical and thoracic cord.

Table 1.

Summary of Notable Serum and CSF Studies for Case Report

	2024			2025
	June	September	October	July
Serum
TNC (cells/μL), (%)	16.3 × 10e3 (19 atypical L)	9.2 × 10e3 (no atypical cells)	Not tested	8.9 × 10e3 (no atypical cells)
HTLV-1 antibodiesa	Not tested	Very strongly positivec	Very strongly positivec	Very strongly positivec
AQP4 IgG (cell-based assay)	Not tested	Negative	Not tested	Negative
MOG IgG (cell-based assay)	Not tested	Negative	Not tested	Negative
Spinal fluid
TNC (cells/μL), (%)	24 (14 L, 70 atypical L)	61 (84 L, 13 atypical L)	Not tested	100 (96 L, 2 atypical L)
Protein (mg/dL)	57	164	Not tested	169
IgG (mg/dL)	Not tested	42.2	Not tested	39.1
IgG index	Not tested	1.02	Not tested	1.12
Oligoclonal bands	Not tested	Present (9 total)	Not tested	Present (10 total)
HTLV-1 antibodiesb	Not tested	Not tested	Not tested	Positived

Abbreviations: AQP4 = aquaporin 4; L = lymphocytes; MOG = myelin oligodendrocyte glycoprotein; TNC = total nucleated cells.

^aScreening ELISA with confirmatory Western blot (ARUP laboratories, test IDs 0051164 and 0020642).

^bScreening enzyme immunoassay with confirmatory line immunoassay (Mayo Clinic, test IDs HTLVC and HTLLC).

^cVery strong reactivity to GD21, p19, p24, p26, p28, p32, p36, p46, p53, and rgp46-I. No reactivity to rgp46-II.

^dReactivity at p19, p24, gp46, gp21.

In the weeks after hospital discharge, her myalgias, cramping, and truncal spasms returned along with worsening paraparesis, gait instability, and sphincter dysfunction. Approximately 1 month after discharge, she was treated for cystitis and completed a 3-day pulse of IVMP from home, followed by a prolonged course of oral prednisone (50 mg daily) without significant symptom relief. Repeat spinal MRI from November 2025, 9 weeks after her initial course of IVMP, and 4 weeks after her second course of IVMP, demonstrated resolution of the cervical cord edema and faint residual T2 prolongation extending from the medullary pyramids through the lateral columns of the cervical and thoracic cord which was associated with faint, patchy enhancement in the lateral columns of the thoracic segments (Figure 1B). Serum HTLV-1 antibodies were again strongly positive (screening ELISA with confirmatory Western blot). She continued prednisone (50 mg daily), and by January 2025, she experienced some improvement in her myalgias and spasms, prompting a gradual decrease in her daily dose of prednisone to 30 mg.

In May 2025, she began taking her prednisone and muscle relaxers sparingly after losing health insurance coverage. Over the following months, her symptoms worsened, and by July 2025, her progressive functional decline prompted return to the hospital. Repeat cranial MRI showed normal brain parenchyma. Repeat spinal MRI demonstrated recurrent cervical cord edema and enhancing T2 prolongation extending contiguously from the medullary pyramids through the conus medullaris which, again, prominently involved the lateral columns (Figure 1C). Repeat serum testing for AQP4 and MOG IgG was again negative, as was repeat paraneoplastic antibody panel and repeat testing for systemic autoantibodies and infection, including metagenomic next generation sequencing ([mNGS], Karius Spectrum). QuantiFERON-Tb Gold was positive, although Mycobacterium tuberculosis PCR was negative, and she had no symptoms, examination findings, or radiographic features suggestive of active tuberculosis. Serum HTLV-1 antibodies were again strongly positive (screening ELISA with confirmatory Western blot). CSF analysis was repeated twice and showed persistent lymphocytosis, elevated protein, and oligoclonal bands (Table 1), as well as positive HTLV-1 antibodies (screening enzyme immunoassay with confirmatory line immunoassay), elevated soluble IL2 receptor, negative AQP4 IgG, and extensive negative testing for lymphoid malignancy, paraneoplastic antibodies, and infection, including mNGS (Delve Detect). CT imaging of the chest and abdomen again showed no evidence of solid malignancy or granulomatous disease. Whole-body PET remained unavailable, although neurosarcoidosis at this point was less favored due to her uncharacteristic spinal MRI findings and lack of symptoms, examination findings, or radiographic findings suggestive of systemic sarcoidosis.

Given her persistent strongly positive HTLV-1 antibodies in the serum and CSF with negative exhaustive testing for alternate infectious, neoplastic, paraneoplastic, metabolic, and autoinflammatory etiologies, she was given a presumptive diagnosis of rapidly progressive HTLV-1–associated myelitis. A 5-day pulse of IVMP resulted in significant improvement in pain and weakness and some improvement in urinary and bowel retention. She was discharged home on prednisone (50 mg daily with prolonged taper) and began treatment for latent tuberculosis by infectious disease consultants. Owing to limitations with insurance and transportation, she has not yet returned for clinical examination or obtained repeat diagnostic testing, though as of November 2025, her daily dose of prednisone has been gradually weaned to 30 mg with stable lumbosacral pain and neurogenic bladder without limb weakness or ambulatory limitations.

Results of Case Review

Including the case presented here, 27 publications containing 45 cases with rapidly progressive or relapsing myelitis caused by HTLV-1 infection were identified in the literature. A detailed summary containing the clinical history, diagnostic evaluation, and treatment details for each of these cases is presented in eTable 1. Patients were predominantly female (67%) and from Japan (56%) or the Caribbean (24%). The median age at presentation was 57 years with a median time from clinical onset to presentation of 5 months. Most patients had rapidly progressive clinical onset (96%), and few experienced clinical relapses either after a rapidly progressive clinical onset (20%) or after a chronically progressive course (4%). Most patients had radiographic features of myelitis (98%), with 91% showing a longitudinally extensive myelitis and 7% showing focal myelitis. There was a single case with normal spinal MRI who experienced rapidly progressive clinical onset with multiple clinical relapses when attempting to wean from steroid therapy. No cases published before 2009 (21 total) reported testing for AQP4 or MOG IgG, and of the remaining 24 cases, 12 (50%) reported testing for AQP4 IgG and 7 (29%) tested MOG IgG. Only 3 cases presented with concurrent or prior optic neuritis, all of whom tested negative for both AQP4 and MOG IgG. Most patients received steroid therapy either as monotherapy (64%) or in combination with an alternate agent (24%). Most patients experienced either clinical or radiographic improvement with treatment (94%), with 79% describing clear clinical improvement and 61% describing clear radiographic improvement, although longitudinal follow-up of these patients was limited.

Rapidly Progressive and Relapsing Myelitis in HTLV-1 Infection

Clinical Course

Although HAM/TSP is classically described as a chronically progressive spastic paraparesis associated with axial pain and sphincter dysfunction in which the infected individual gradually accrues debility in a nonremitting fashion over years,^19,20 cases of rapid-onset HAM/TSP have been reported in the literature,^21-24 with multiple studies describing rapid progression in 6%–26% of patients with confirmed HAM/TSP.^14,25-29 Rapid progression in HAM/TSP is commonly defined as reaching ambulatory failure within 2 years of clinical onset,^14,25,29 although this decline is often heralded by an acute to subacute progression evolving over weeks to months.^{15-17,21,22,24,30-37} Despite reaching a nadir after the initial rapidly progressive course (or partial remission in some cases^21,22,30,37), if followed longitudinally, many of these patients will experience a chronically progressive spastic paraparesis^15,21,25 with a rate of functional decline greater than that of patients with classic HAM/TSP³⁸ and very rare cases of relapsing myelitis.^{15,21,31,39,40} Although the most common HTLV-1–associated ocular diseases in HAM/TSP are uveitis and keratoconjunctivitis,⁴¹ a chronic optic neuropathy is observed in many cases of HAM/TSP⁴² and rare reports of optic neuritis with or without myelitis have been described with inconsistent or incomplete testing for antibodies to AQP4 or MOG in such cases.^15,43-45

Diagnostic Evaluation

The diagnosis of HAM/TSP is made when a patient with a compatible clinical course and reasonable exclusion of alternate diagnoses is found to have serum and CSF positivity for HTLV-1 antibodies (usually screening enzyme immunoassay with confirmation through Western blot or line immunoassay) and/or HTLV-1 proviral DNA (confirmed via PCR).²⁰ Compared with patients with slowly progressive HAM/TSP, those with rapidly progressive disease have a more inflammatory spinal fluid profile (increased leukocytes, oligoclonal IgG bands, and elevated levels of protein, CXCL10, and neopterin) with increased CSF to serum ratio of HTLV-1 antibodies.^14,29,32

Nearly all described cases of rapidly progressive or relapsing myelitis in HAM/TSP are associated with diffuse or focal signal abnormalities on spinal MRI (Table 2), which may lead to an initial diagnosis of multiple sclerosis (MS)⁴⁶ or NMOSD.^15,33,43 These imaging findings are often identified early in the clinical course, although focal, diffuse, and enhancing cord lesions have also been observed years after clinical onset during either a relapsing^15,39 or nonrelapsing^47-49 chronic progressive course. High HTLV-1 proviral load in the serum or spinal fluid⁴⁶ and the absence of antibodies to AQP4 or MOG^15,33,43,45 are helpful in distinguishing these patients from those with MS, NMOSD, and MOGAD infected with HTLV-1, although many cases reported in the literature do not report testing for these antibodies or were published before the commercial availability of this testing, and commercial testing for quantitative HTLV-1 PCR is unavailable in certain countries (including the U.S.). Myelitis symmetrically involving the pyramidal tracts and contiguously spanning multiple spinal segments is observed histopathologically in HAM/TSP^50,51 and is a recently described radiographic biomarker of rapidly progressive HAM/TSP,¹⁵ which was observed in our patient. These radiographic findings are helpful in distinguishing these patients from NMOSD,¹⁵ although the presence of similar findings in paraneoplasia⁵² necessitates testing for paraneoplastic antibodies and surveillance of occult malignancy in such patients.

Table 2.

Clinical, Laboratory, and Treatment Data for Published Cases of Rapidly Progressive and Relapsing HAM

	Total (n = 45)
Demographics
Age (y)	57 (50–65)
Sex (F), (%)	30 (67)
Nativity, (%)
Japan	25 (56)
Caribbean or South America	14 (31)
Other or not reported	6 (13)
Clinical course
Clinical onset to presentation (mo)	5 (3–10)
Rapid onset, (%)	34 (76)
Rapid onset and relapsing, (%)	9 (20)
Chronic progressive and relapsing, (%)	2 (4)
Serum studies, (%)
HTLV1 positivitya	44 (98)
AQP4-IgG not testedb	33 (73)
MOG-IgG not testedb	38 (84)
Spinal fluid studies
HTLV1 positivitya, (%)	41 (91)
Cells (n = 32)	10 (3–35)
Protein (n = 11)	58 (51–75)
IgG (n = 9)	9 (8–14)
IgG index (n = 6)	1.0 (0.8–1.3)
OCB (n = 17), (%)	4 (29)
Spine imaging, (%)
Abnormal cord imaging	44 (98)
Longitudinally extensive lesion	41 (91)
Focal lesions	3 (7)
Treatment (n = 33), (%)
Steroid monotherapy	21 (64)
Steroid + other	8 (24)
IFNα monotherapy	2 (6)
Unspecified	2 (6)
Response to treatment, (%)
Clear clinical improvement	26 (79)
Radiographic improvement	20 (61)
Any clinical or radiographic improvement	31 (94)

Abbreviations: AQP4 = aquaporin 4; HAM = HTLV-1–associated myelopathy; MOG = myelin oligodendrocyte glycoprotein; OCB = oligoclonal bands.

Results are reported as median (interquartile range) or n (%) unless otherwise stated.

Spinal fluid cells are reported as total per μL; protein and IgG levels are reported as mg/dL.

^aHTLV1 testing in serum or CSF was any reported positive test (PA, ELISA, PCR, Western blot).

^bAQP4-IgG and MOG-IgG were negative in all tested cases (any positive cases excluded from analysis).

While nonspecific, the presence of atypical lymphocytes in the serum and CSF⁵³ and infective dermatitis⁵⁴ are both well-recognized features of HTLV-1 infection¹⁹ that have been described in HAM/TSP^47,55 and may have been early diagnostic clues for our patient. Given the rarity of rapid onset HAM/TSP and that the most recently proposed modifications to the original World Health Organization (WHO) diagnostic criteria for HAM/TSP do not incorporate typical MRI findings for either classic or rapidly progressive disease,^14,20 sufficient exploration of alternate diagnoses is advised for each of these patients on a case-by-case basis with particular focus on testing for AQP4-IgG, MOG-IgG, granulomatous disease, paraneoplastic antibodies, malignancy, and exposure-relevant infectious myelopathies (e.g., HIV, Treponema pallidum, Schistosoma mansoni, and Mycobacterium tuberculosis are pathogens which can present with myelitis and share risk factors or geographic distribution with HTLV-1 infection).

Treatment

While most patients with HAM/TSP benefit from individualized symptomatic and supportive care (e.g., physiotherapy, antispasmodics, bowel and bladder hygiene, ambulatory assistive devices), there are limited high quality data to guide the selection of long term of disease-modifying therapy. There are trial data describing modest functional improvement with the use of interferon α,⁵⁶ although given the intolerability and limited long term clinical benefit, its regular use has fallen out of favor and is no longer recommended as a first line therapy in HAM/TSP.¹⁸ There are also trial data which describe favorable clinical response to the use of glucocorticoids, with the greatest benefit observed in patients with rapidly progressive disease who received initial high dose rather than low dose maintenance steroid.⁵⁷ While radiographic biomarkers of rapidly progressive and relapsing HAM/TSP have not been incorporated into prior treatment trials, review of available published cases demonstrates that most of these patients are treated with glucocorticoids, occasionally in combination with other therapies, and that greater than 90% of treated patients will experience clinical or radiographic improvement (often both, Table 2 and eTable 1).

Current consensus-based guidelines recommend that all patients with progressive disease (including rapid and slow progressors) are offered pulse steroid followed by maintenance therapy, usually consisting of low dose oral prednisone for a period of up to 4 years, and that some patients require prolonged courses given clinical deterioration when attempting to wean from steroid.¹⁸ Given that rapid progressors eventually experience chronically progressive clinical deterioration and spinal cord volume loss despite initial clinical and radiographic improvement with steroid, these patients may especially benefit from early and aggressive targeted immunomodulation.¹⁸ The development of a steroid-sparing immunomodulatory therapy to target the pathogenesis and compartmentalized chronic inflammation in HAM/TSP is an ongoing international research effort, with various proposed candidate therapies including CCR4 antagonism,⁵⁸ B-cell depletion,⁵⁹ and inhibition of pyrimidine synthesis⁶⁰ (see also trial ID# NCT04799288) among others.

Glossary

AQP4

assays for aquaporin 4

HTLV-1

human T lymphotropic virus type 1

mNGS

metagenomic next generation sequencing

MOG

myelin oligodendrocyte glycoprotein

MOGAD

myelin oligodendrocyte glycoprotein antibody associated disease

MS

multiple sclerosis

NMOSD

neuromyelitis optica spectrum disease

Author Contributions

A.A. Morrison: drafting/revision of the manuscript for content, including medical writing for content; major role in the acquisition of data; study concept or design; analysis or interpretation of data. R.D. Samudralwar: drafting/revision of the manuscript for content, including medical writing for content. J.R. Berger: drafting/revision of the manuscript for content, including medical writing for content; study concept or design.

Study Funding

The authors report no targeted funding.

Disclosure

A.A. Morrison: no disclosures R.D. Samudralwar: scientific advisory or data safety monitoring board for EMD Serono, TG Therapeutics, Genentech, and Amgen. J.R. Berger: consultancies for Celgene/BMS, Cycle Pharma, Dice Therapeutics, Genentech/Roche, Gilead, Janssen/J and J, Merck, Morphic, Novartis, Sandoz, Seagen, Takeda, Population Bio, Excision Bio, and TG Therapeutics. He is on the DSMB of MAPI. He also speaks on behalf of TG Therapeutics. Go to Neurology.org/NNfor full ddisclosures.