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Frontiers in Virology ·

Volume 6 - 2026 | https://doi.org/10.3389/fviro.2026.1807017

Persistent low-level HIV viremia: a narrative review of diagnostic predicaments, virological pathomechanisms, and clinical outcomes

  • Shanmugam Saravanan1*corresponding author
  • Ramachandran Vignesh2*corresponding author
  • Madhavan Vidya3
  • Sathasivam Sivamalar4
  • Pachamuthu Balakrishnan4
  • Esaki M Shankar5
  • Marie Larsson6*corresponding author
  1. 1Dental Research Cell, Dr. D. Y. Patil Dental College & Hospital, Dr. D.Y. Patil Vidyapeeth (Deemed to be University), Pune, Maharashtra, India
  2. 2Pre-Clinical Department, Faculty of Medicine, Royal College of Medicine Perak, Universiti Kuala Lumpur, Ipoh, Malaysia
  3. 3Aevum Bio Labs Pvt Ltd., Hyderabad, India
  4. 4Department of Research, Meenakshi Academy of Higher Education and Research (MAHER), Chennai, India
  5. 5Infection and Inflammation, Department of Biotechnology, School of Integrative Biology, Central University of Tamil Nadu, Thiruvarur, India
  6. 6Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology, Linköping University, Linköping, Sweden
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Abstract

Despite major strides made with combination antiretroviral therapy (cART), people living with HIV (PLHIV) continue to face higher mortality rates compared to the general population. A significant part of this gap stems from non-communicable diseases arising from chronic immune activation. While the primary goal of treatment is to suppress the virus to undetectable levels, typically below <20 to <75 copies/mL depending on the assay used, many patients still show low-level viremia (LLV), where HIV RNA persists below the threshold for virologic failure (<1,000 copies/mL). LLV is important in clinical care, yet its definition varies widely across guidelines, and its real-world impact largely depends on the magnitude and persistence of viremia. Studies show that viral blips and persistent low-level viremia (pLLV) should be distinguished. Transient blips are generally not associated with adverse outcomes, whereas pLLV, particularly at levels >200 copies/mL, has been linked to increased risks of virologic failure and drug resistance across different cohorts. However, the findings are heterogeneous, particularly among those with LLV ranging from 50 to 199 copies/mL. Recent evidence suggests that much of the persistent viremia during suppressive ART results from clonally expanded infected CD4+ T cells rather than from ongoing, complete cycles of viral replication. Current guidelines do not recommend routine ART modification for LLV <200 copies/mL; instead, they prioritize adherence assessment, repeat viral load monitoring, and resistance testing when feasible. There is limited evidence supporting regimen modification, which remains restricted to patients with persistent viremia >200 copies/mL, particularly when resistance mutations are detected. This review critically synthesizes current evidence on the definitions, epidemiology, clinical impact, mechanisms, diagnostic approaches and practical management of LLV with a focus on differences in data, challenges, and outcomes between low- and middle-income countries (LMICs) and high-income countries (HICs). It also highlights controversial areas and research priorities.

Keywords

1 Introduction

Human immunodeficiency virus (HIV) patients receiving combination antiretroviral therapy (cART) continue to experience higher mortality rates than the general population, despite considerable improvements in survival rates (1). Although the overall frequency of AIDS-related deaths has been steadily declining, the proportion of people living with HIV (PLHIV) fatalities attributable to noncommunicable diseases is on the rise and vast majority of these diseases are increasingly reported among PLHIV than in the general population (2). The underlying causes are multifactorial and not fully understood, but likely involve a combination of a higher prevalence of traditional risk factors, toxicity associated with antiretroviral (ARV) drugs, and persistent immune activation and inflammation associated with HIV infection (3, 4).

Achieving virologic suppression (VS) in individuals taking cART is the primary goal of modern HIV treatment (5–7). But the definitions of VS vary across countries based on the assay sensitivity, healthcare resources and clinical priorities. According to current US Department of Health and Human Services (DHHS) guidelines, VS is generally defined as a viral load (VL) value consistently below the lower limit of quantification of the commercial assay used (typically <20 - <75 copies/mL, depending on assay sensitivity) (8). Similarly, the European AIDS Clinical Society (EACS) considers VS as HIV RNA below 50 copies/mL using standard clinical assays (7). In contrast, the World Health Organization (WHO) uses a higher threshold, defining suppression as a viral load <1000 copies/mL, mainly to guide pragmatic clinical and public health decision-making in resource-scarce settings (9). Adequate VS has the potential to lessen the spread of HIV, improve clinical outcomes, and halt the evolution of resistance mutations (10). While a majority of patients complying with the recommended ART regimens attain VS, the plasma viral RNA remains detectable at levels below the threshold (for virologic failure) in a minor proportion of individuals, a phenomenon identified as low-level viremia (LLV) (11). Although substantial evidence associates elevated HIV RNA levels with mortality, AIDS, and serious non-AIDS events (SNAEs), the impact of LLV on clinical outcomes is still unclear (11, 12). It remains challenging to determine whether LLV reflects transient biological fluctuations, issues with adherence, resistance, or persistent viral production from long-lived infected cells.

2 Definitions and epidemiology

LLV is a major challenge in monitoring the health of PLHIV, along with optimizing their treatment (5–7, 11, 12). Because LLV is defined relative to VS thresholds, variations in those thresholds across international guidelines lead to differences in how LLV is defined and managed clinically. The EACS generally classifies LLV as detectable VL above the assay limit (>51 copies/mL) but in the <200 copies/mL range (7). Similarly, the DHHS defines LLV as 50 to 200 copies/mL (5). In contrast the WHO, whose recommendations are widely followed in low- and middle-income countries (LMICs), adopts a wider definition, categorizing LLV between 50 and 999 copies/mL (6).

LLV has been further categorized into distinct patterns of behavior over time, namely viral blips and persistent low-level viremia (pLLV). Viral blips are defined as isolated episodes of detectable viremia (isolated VL of >50–999 copies/mL) that are preceded and followed by VS and are generally considered clinically benign (5–7). In contrast, pLLV refers to repeated or sustained detectable viral loads (VLs of 50–999 copies/mL) on two or more consecutive measurements, indicating ongoing low-level viral replication (5–7). Key differences in definitions and management approaches across major guidelines are summarized in Table 1.

Table 1. Definitions of low-level viremia and recommended management strategies across major HIV treatment guidelines.

GuidelineDefinition of LLVVirologic failure (VF) thresholdApproach to LLV <200 copies/mLApproach to persistent LLV >200 copies/mLResistance testing recommendations
WHO50–999 copies/mL≥1000 copies/mL (2 consecutive values)Adherence counseling; repeat VL in 3 months.Switch regimen after confirmed VL>1000 copies/mL on two consecutive measurements following adherence interventionRecommended at confirmed VF; not routinely at lower VL
DHHS50–200 copies/mL≥200 copies/mLConfirm adherence; repeat VL; no routine ART changeEvaluate for VF; consider resistance testing and regimen modificationRecommended for >200 copies/mL; may be unsuccessful at low VL
EACSDetectable VL above assay limit (>51 copies/mL) but <200≥200 copies/mLReinforce adherence; repeat VL; monitor trendsIndividualized approach; consider resistance testing and modification if persistentRecommended when feasible. Especially >200 copies/mL
Delphi Consensus (2024)No fixed cut-off; emphasizes persistence and clinical contextContext-dependentAdherence assessment; repeat testing; avoid routine modificationRisk-stratified approach; consider modification if persistent >200 with risk factorsCase-based; consider RNA ± proviral DNA testing depending on feasibility

VL, viral load; LLV, low-level viremia; VF, virologic failure. Definitions and management approaches vary across guidelines and should be interpreted in clinical context.

Although not formally defined in guidelines, many observational studies have subclassified LLV into finer categories, including very low-level viremia (VLLV; typically <50 copies/mL) (13, 14) and low-level viremia (50–200 copies/mL) (15–20), with some additionally defining higher-level LLV (200–999 copies/mL) (15–17, 19, 20). This classification shows a spectrum of clinical risk, with increasing viral load associated with a higher likelihood of adverse outcomes.

The global prevalence of LLV remains poorly characterized and varies considerably across settings, as summarized in Table 2. Pooled global estimates suggest that LLV occurs in approximately 13–14% of individuals on ART, while individual cohort studies show substantial variability (7–30%), influenced by differences in viral load thresholds, frequency of monitoring, duration of follow-up, and population characteristics (15, 18, 21–23). In HICs settings, with stricter thresholds and more frequent viral load testing, LLV prevalence is generally lower, at 5% to 15% (5, 7, 15, 24). Studies from LMICs following WHO recommendations present higher estimates, between 15% -20% (25). In addition to variations in definitions, factors such as differences in access to viral load monitoring, adherence support, resistance testing, and the availability of second-line regimens influence the prevalence of LLV in HICs and LMICs (6, 19). Particularly in the LMIC settings, prolonged duration of unrecognized LLV could be due to the delay in detecting virological failure in addition to the limited access to resistance testing, thereby further increasing the risk of resistance development and adverse outcomes (26–28).

Table 2. Epidemiology of low-level viremia in people living with HIV across global settings.

SettingLLV definition usedPrevalenceStudy featuresReferences
HICs (High-income countries)
High-income countries (Western settings)50–200 copies/mL (DHHS, EACS)~5–15%Frequent monitoring, sensitive assays(15, 24)
LMICs (Low- and middle-income countries)
LMICs (overall)50–999 copies/mL (World Health Organization)~15–20%Broader definition; higher observed burden; influenced by monitoring strategies(25)
IndiaChennaiWestern India(DTG cohort)<1000 copies/mL (WHO-aligned)20–200 copies/mL15.2%12.9–23.3% (time-point dependent)3498 patients; stratified LLV (40–999 copies/mL)LLV at 6, 12, 18 months: 17.9%, 12.9%, 23.3%; persistent LLV 2.9%(19) (18)
Asia50–999 copies/mL (WHO-aligned)~11-12%Moderate prevalence; consistent with LMIC trends(23)
Sub-Saharan AfricaWHO-based~18–22%Higher burden, adherence and access challenges(32)
Global
Individual cohort studies (global)Study-specific~7–30%Includes both Western and LMIC cohorts; variability due to definitions, monitoring, and population differences(15, 18, 22, 23)
Global (pooled estimates)Varies (50–200 or 50–1000 copies/mL)~13–14%Meta-analysis; high heterogeneity(21)

VL, viral load; LLV, low-level viremia. The prevalence of LLV varies considerably across settings, showing broader definitions and differences in monitoring practices.

In the western India cohort, LLV among dolutegravir-experienced patients was reported in a time-dependent manner, with frequencies ranging from 12% to 23% over 6–24 months of follow-up, using a definition of 50–200 copies/mL. But most episodes were transient, with persistent LLV observed in only 2.9% of individuals (18). In contrast, a large cohort study from Chennai reported a higher LLV prevalence of 15.2%, using a higher threshold of 50–999 copies/mL (19). This difference likely reflects variation in LLV thresholds, with narrower definitions potentially underestimating the overall burden. These findings show variation in LLV reporting even within the same country due to differences in definitions and suggest that LLV is relatively common in Indian cohorts. This points to the need for contextual and longitudinal assessment rather than relying solely on single viral load thresholds (11, 26, 29–31).

3 Clinical impact

The link between LLV and VF remains the most debated aspect. Multiple cohort studies have shown that persistent LLV at or above 200 copies/mL confers a higher risk of subsequent virologic failure (12, 20, 29, 33–36), a threshold incorporated into clinical guidelines in high-income settings such as those from DHHS (5) and EACS (7). A large Cohort study from southern India demonstrated that, compared to fully suppressed patients (PVL < 40 copies/mL), those with LLV had a greater risk of VF, and this risk increased with higher LLV levels (19). Consistent evidence from other LMIC settings, including cohorts from Asia and sub-Saharan Africa, confirms the conclusion that LLV, particularly at levels ≥200 copies/mL, is an independent predictor of subsequent virologic failure (20, 25, 32, 33). A recent systematic review and meta-analysis further confirms this heterogeneity, showing that the prognostic significance of LLV is not uniform, but is determined through various factors, including duration of viremia, ART regimen, baseline resistance, and adherence levels (31). Other recent reviews also emphasize that LLV should be approached as a dynamic clinical state rather than a fixed virological category (26).

Beyond virologic outcomes, LLV has also been linked to adverse clinical endpoints. A longitudinal study by Ola Elvstam et al. demonstrated an association between LLV and increased all-cause mortality, particularly at higher viral load levels (11). Furthermore, the AFRICOS study shows that pLLV has been associated with an increased burden of non-infectious comorbidities, including cardiovascular and metabolic conditions (32). These data suggest that ongoing low-level viral replication may contribute to chronic immune activation and inflammation.

However, the clinical relevance of persistent viremia in the 50–199 copies/mL range is less well defined. This level of LLV either had a statistically insignificant risk of VF (35) or the risk of VF was modest when compared to higher LLV categories (37). Some studies suggest LLV at this level may reflect assay variability, residual virus release from reservoirs or transient immune activation and hence the clinical relevance is unclear (38). Notably, not all LLV carries the same clinical risk. Viral blips, which are transient episodes of detectable viremia, are generally considered clinically benign and may reflect temporary lapses in adherence or assay variability (5, 15). But according to a recent study, detectable viremia in the range 51 to 199 copies/mL, both viral blips and pLLV was associated with subsequent virologic failure (39). Collectively, these outcomes stress that the clinical impact of LLV is strongly influenced by its persistence and magnitude, with sustained or higher-level viremia representing a key risk factor for adverse outcomes. In LMIC settings, delayed HIV diagnosis and late ART initiation frequently result in low baseline CD4 counts and higher pre-treatment viral loads, both of which are strong predictors of suboptimal immune recovery and are independently associated with an increased likelihood of persistent LLV (29, 35, 40). Additionally, a high burden of coinfections such as tuberculosis further amplifies immune activation, which in turn promotes residual viral replication and sustains LLV (11, 16, 17). Persistent LLV has been observed to be associated with ongoing immune activation and inflammation which may further contribute to non-AIDS comorbidities (31). Chronic low-level antigenic stimulation could sustain CD4+ T cell turnover and immune dysregulation leading to maintenance of viral reservoirs and limiting immune recovery (41–43).

4 Mechanisms of persistent low-level viremia

Multiple factors have been observed to be associated with LLV, including non-adherence, resistance mutations, use of protease inhibitors (PI), lower CD4+ baseline nadir counts (below 200 cells/mm3), higher baseline viral loads (1,000,000 copies/mL), shorter duration of viral suppression prior to ART switch from PI to integrase strand transfer inhibitor (INSTI), prior exposure to mono or dual therapy, age above 50 years, black race and male gender (11, 23). However, these associations do not necessarily imply causation of the underlying mechanism. Findings from several studies increasingly support the view that persistent viremia during otherwise suppressive ART frequently reflects virus production from long-lived clonally expanded CD4+ T cells rather than ongoing rounds of full viral replication (14, 44–46). The relative genetic stability of plasma virus during suppressive therapy, along with the failure of intensification studies to significantly reduce residual viremia in most patients, supports this interpretation (47–50). However, these data do not rule out all ongoing replication, as limited replication in sanctuary sites with poor drug penetration remains biologically plausible, and resistance may emerge in some cases. In certain cohorts, PI-based regimens have been linked to LLV, which may reflect treatment history and reservoir size as much as direct pharmacologic effects (12, 15, 29, 36). Therefore, mechanistic interpretation should be individualized and should not automatically prompt treatment intensification.

Recent studies suggest that persistent low-level viremia (pLLV) arises from multiple biological processes, including clonal viral production, and is variably influenced by anatomical and pharmacological factors (26).

5 Role of adherence and drug resistance

Adherence is a significant factor and the primary concern to address when LLV is detected (5, 13, 31). Poor or intermittent adherence in patients leads to an increased risk of treatment failure when there is a low level of viremia (34, 51). Evidence from high-income settings shows a strong association between suboptimal adherence and the development of class-specific resistance mutations (52). In LMICs, where treatment monitoring and resistance testing may be less frequent, the gaps in adherence contribute substantially to the rising burden of HIV drug resistance globally (53, 54). However, a stable LLV in a patient with regular adherence, without documented resistance, raises the possibility of reservoir-driven virus production (55). It should be noted that current evidence does not support routine ART modifications for every episode of LLV (5, 31). Intensification strategies, including the addition of the CCR5 antagonist maraviroc, have demonstrated inconsistent or limited benefits and should not be interpreted as establishing a general management principle (47–49, 56). Pooled analyses indicate that the risk associated with LLV is strongly influenced by adherence and resistance profiles and virological thresholds alone are not sufficient to guide management decisions (31).

6 Diagnostic challenges

Conventional Sanger sequencing-based genotypic resistance testing is most reliable when plasma viremia is sufficiently high to allow accurate RNA amplification, typically at viral loads >1,000 copies/mL (5, 6, 57). In routine clinical practice, these assays may fail or yield incomplete results at lower viral loads, below 500–1,000 copies/mL, depending on the laboratory and testing platform (51). To improve assay sensitivity at LLV, enhanced methods such as increased plasma input volume, ultracentrifugation to concentrate viral particles, or nested PCR have been explored; however, these methods are not widely available in all clinical settings (57).

When amplification is successful at LLV, interpretation is still a challenge, as detected resistance mutations may represent either newly emerging variants under selective drug pressure or archived mutations from prior, failed treatment regimens (57, 58). Nevertheless, clinically meaningful information can still be obtained, particularly in specialized centers where results are interpreted alongside detailed treatment history and prior resistance data (31).

When plasma RNA genotyping is unsuccessful or unavailable, proviral DNA genotyping may provide complementary information, but its interpretation requires caution, as proviral DNA may include defective viral genomes and historical resistance mutations that are no longer clinically relevant, potentially leading to overestimation or misrepresentation of the current resistance profile (31).

Next-generation sequencing (NGS) offers even greater sensitivity for detecting minority variants, but its clinical role in LLV remains incompletely defined, as prospective evidence indicates that improvements in patient outcomes are limited (51, 59). Thus, diagnostic escalation from RNA genotyping to proviral DNA testing or NGS should be considered a case-based strategy rather than a universal recommendation (31). These shortcomings in diagnostic sensitivity and interpretation are now recognized as key challenges in LLV management, especially as ART regimens evolve and viral load assays become more advanced (26).

7 Clinical management and practical guidance

A practical approach should begin by confirming the pattern of viremia. In the case of a single viral load in the LLV range, especially following prior suppression, clinicians should primarily evaluate adherence, comorbidities, drug-drug interactions, nutritional requirements, and potential laboratory variability. Then, it is advisable to repeat the viral load measurement within an appropriate interval (5–7). In patients with pLLV and a viral load of <200 copies/mL, current DHHS and transmission-prevention guidance generally favor persistent monitoring and reinforcement of medication adherence, rather than an immediate change in the regimen (5). A recent Delphi consensus offers systematic guidance for this scenario, prioritizing adherence assessment and repeat viral load monitoring as primary interventions. ART modification is generally not recommended for low-level viremia below 200 copies/mL unless resistance is detected (60). In contrast, closer evaluation is warranted for those with persistent viremia>200 copies/mL, given the risk of VF and the higher incidence of resistance in this population (11, 51). The same consensus endorses a risk-stratified approach, recommending regimen modification only for persistent viremia of at least 200 copies/mL, especially when documented resistance or additional high-risk features are present.

Blips and very low-level viremia should not be managed as persistent viremia, since isolated blips that quickly return to undetectable levels are not an indication to switch therapy (5, 13). Likewise, detectable HIV RNA below the limit of quantification is interpreted as assay-detectable but clinically low-risk viremia in a patient whose infection is otherwise controlled. These scenarios warrant confirmation of adherence and follow-up testing rather than escalation of therapy (5, 6). Clear communication with patients is key to avoiding overinterpretation of isolated detectable values as treatment failure. Regimen modification may be appropriate in cases of persistent LLV accompanied by documented resistance, increased viral load or other high-risk features, ideally with expert input (13, 39). It should be noted that evidential indications suggesting a possible benefit in selected patients should be distinguished from guideline-based routine practice. And this is especially important in settings that still define virological failure at >1000 copies/mL, because programmatic thresholds for action do not necessarily imply biological equivalence across all viral load categories (6, 61).

8 Transmission implications and U=U

The idea that ‘Undetectable = Untransmittable’ (U=U) is strongly supported by evidence showing that sexual transmission of HIV does not happen when plasma viral load stays consistently below 200 copies/mL. This cut-off is based on large studies such as PARTNER, Opposites Attract, and HPTN052, which found no linked transmissions below this level (10, 62, 63). For people with low-level viremia (LLV), current research indicates that the risk of transmission is extremely low when viral loads are below 200 copies/mL, even though sensitive tests can still detect the virus (10, 62). There is less evidence for higher viral loads, so it is important to be careful when applying these outcomes above this threshold (31, 61, 64). In practice, people with persistent low-level viremia (pLLV) under 200 copies/mL can be counseled according to U=U principles, provided adherence is maintained, and regular virologic monitoring occurs (65). Explicit communication of this threshold is essential, especially in settings where higher cut-offs, such as over 1000 copies/mL, are used to define virological failure (64). It is to be noted that while plasma viral load is considered an important determinant of transmission risk, a few studies of genital tract compartments, point out that HIV RNA may occasionally be detected in spite of effective ART, demonstrating discordance between compartments (66, 67). For example, rectal swab studies in MSM found that a small proportion of men with low plasma viral loads (<1000 copies/mL) still had detectable HIV in rectal secretions (66). Cervical shedding has likewise been reported among individuals with low or undetectable plasma viral loads (<500 copies/mL), underscoring concerns about mucosal compartmentalization (67). That study also found greater genital shedding with NNRTI-based regimens compared with protease inhibitor regimens, suggesting a link between low local drug concentrations and compartmentalized replication. However, this does not translate into measurable transmission risk when plasma viral load is suppressed (68, 69).

Nonetheless, people living with HIV who experience LLV may engage in risk behaviors because they perceive themselves as noninfectious (70), which highlights the need for continued monitoring and preventive measures, especially given the documented risk of subsequent virologic failure in the LLV group.

Figure 1 integrates definitions, mechanisms, diagnostic pathways, and a proposed clinical management framework for LLV.

Schematic overview of LLV definitions across guidelines, proposed mechanisms of persistent viremia, diagnostic options and a practical management pathway.
Figure 1. Schematic overview of LLV definitions across guidelines, proposed mechanisms of persistent viremia, diagnostic options and a practical management pathway.

9 Limitations

The first limitation is that it is a narrative review and does not employ a systematic search strategy or study selection criteria, which may introduce selection bias and limit reproducibility. Secondly the review is based on observational data and does not have standardized quality assessments of studies included. A narrative approach was chosen due to the limited availability of standardized data, particularly from LMICs, and the absence of uniform definitions across studies, to provide a clinically meaningful overview and at the same time, highlight areas requiring further systematic investigation.

10 Conclusion

Persistent low-level viremia represents a heterogeneous clinical condition that necessitates individualized interpretation and management. Evidence reliably shows an increased risk of virologic failure and resistance when persistent viremia is at or above 200 copies/mL (14, 39). In contrast, the clinical significance of viremia levels between 50 and 199 copies/mL remains unclear and is highly context dependent (35, 37, 39). Recent systematic reviews and expert consensus statements indicate that the clinical implications of low-level viremia are determined by multiple factors, such as the duration of viremia, patient adherence, resistance patterns, and the specific treatment regimen, rather than viral load thresholds alone (26, 31, 60).

Crucially, the interpretation and management of LLV differ across settings. In high-income countries, access to sensitive viral load assays, resistance testing, and individualized clinical care allows for closer monitoring and earlier intervention (15, 24, 39). On the other hand, in LMICs, where resource restrictions and constrained access to resistance testing influence clinical decision-making, resource-adapted clinical approaches are frequently used, with management strategies prioritizing adherence interventions instead of immediate regimen modification (6, 25, 32). These contextual differences point to the need for setting-specific tactics while maintaining a uniform evidence base.

Although the Delphi consensus (60) acknowledges constraints on LMIC care, panels are frequently dominated by experts from high-income settings, which may limit contextual relevance. Greater representation from sub-Saharan Africa and Asia is needed to represent real-world problems such as supply chain limitations and constrained access to second-line therapies, alongside a stronger emphasis on public health–oriented virologic failure thresholds (e.g., >1000 copies/mL) as recommended by the World Health Organization.

Future efforts should standardize definitions, conduct large prospective studies on management strategies, improve validation of RNA and proviral DNA resistance testing at lower viral loads, and further investigate reservoir biology as a key driver of persistent viremia. Current WHO-defined thresholds may fail to capture clinically meaningful LLV and it remains unclear whether thresholds derived mainly from HIC data are directly applicable to LMIC settings.

Ultimately, optimizing the identification and management of LLV across both HIC and LMIC settings will be essential for sustaining long-term treatment success and achieving global HIV control targets, including the UNAIDS 95–95–95 goals.

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Footnotes

Edited by: Karen M Duus, Touro University Nevada, United States

Reviewed by: Sandra Milena Gonzalez Diaz, Public Health Agency of Canada (PHAC), Canada

Rossana Scutari, University of Milan, Italy

Statements

Conflict of interest

MV was employed by Aevum Bio Labs Pvt Ltd.

The remaining author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

The authors ES and ML declared that they were an editorial board member of Frontiers at the time of submission. This had no impact on the peer review process and the final decision.

Funding

The author(s) declared that financial support was received for this work and/or its publication. Dr. Marie Larsson is supported by the Swedish Research Council Project Grant (2021–02703), Region Östergötland Research Project Grant and MIIC Grant.

Author contributions

SMS: Data curation, Methodology, Writing – review & editing, Conceptualization, Validation, Supervision, Writing – original draft, Resources, Visualization. RV: Visualization, Data curation, Resources, Validation, Writing – review & editing, Methodology, Supervision, Writing – original draft. MV: Conceptualization, Supervision, Validation, Writing – review & editing, Writing – original draft, Data curation. SSS: Validation, Supervision, Methodology, Writing – review & editing, Writing – original draft. PB: Supervision, Writing – review & editing, Conceptualization, Writing – original draft, Validation. ES: Conceptualization, Writing – original draft, Visualization, Writing – review & editing, Validation, Supervision. ML: Writing – review & editing, Validation, Supervision, Resources, Methodology, Writing – original draft, Visualization.

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Citation

Saravanan, S., et al. (2026). Persistent low-level HIV viremia: a narrative review of diagnostic predicaments, virological pathomechanisms, and clinical outcomes. Frontiers in Virology, Volume 6. https://doi.org/
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Copyright © 2026 Saravanan, Vignesh, Vidya, Sivamalar, Balakrishnan, Shankar and Larsson.

License: https://creativecommons.org/licenses/by/4.0/

*Correspondence: Shanmugam Saravanan; Ramachandran Vignesh; Marie Larsson

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