Clinical Features of AIDS

Slide 1 · Clinical Features of AIDS

HIV infection: patterns of advanced immune deficiency

Opportunistic infections · HIV-associated neoplasms · Neurologic disease · Clinicopathologic effects of therapy

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Recognize major AIDS presentations and the patterns of opportunistic infection.

Connect severe immune deficiency to characteristic infectious and neoplastic complications.

Explain the histopathologic evolution of lymphoid tissues in HIV infection.

Assess how antiretroviral therapy changes morbidity and clinical presentation.

Slide 3 · AIDS represents the terminal clinical phase of untreated HIV infection

Acute HIV infection

Chronic HIV infection

Advanced immune deficiency / AIDS

Early viremic illness with dissemination

Ongoing viral replication and progressive CD4+ T-cell loss

Opportunistic infections, selected tumors and neurologic disease

Slide 4 · Clinical presentation is multisystemic

Constitutional: Prolonged fever, weight loss and generalized lymphadenopathy.

Gastrointestinal: Persistent diarrhea, opportunistic esophagitis and colitis.

Infectious: Multiple pathogens can affect several organs simultaneously.

Neurologic and neoplastic complications may dominate the presentation.

Slide 5 · Untreated AIDS and the ART era

Untreated or poorly controlled infection

Progressive CD4+ T-cell depletion

High frequency of severe opportunistic infections

Marked risk of selected oncogenic-virus tumors

Effective antiretroviral therapy

Reduced viremia and progressive immune restoration

Major decline in many classic AIDS events

Greater prominence of chronic non-AIDS morbidity

Slide 6 · Clinical spectra vary geographically

The distribution of opportunistic agents is shaped by regional pathogen exposure.

Tuberculosis is a particularly important contributor to AIDS mortality globally.

Availability and effectiveness of ART strongly modify observed case mixes.

Historical pre-ART percentages should not be generalized to treated populations.

Slide 7 · Why opportunistic infections emerge

Latent or low-virulence organism

Loss of cell-mediated immune containment

Reactivation or disseminated infection

Organisms may persist despite previous immune control

Advanced CD4+ T-cell dysfunction reduces pathogen surveillance

Organ-specific symptoms or multi-organ disease become clinically apparent

Slide 8 · Sources of infection in AIDS

Reactivation of latent infection

Pneumocystis jirovecii (source describes reactivation)

Cytomegalovirus or herpesviruses

Tuberculosis and toxoplasmosis

Opportunistic exposure / acquisition

Environmental fungi and other microorganisms

Enteric protozoa and bacteria

Primary infection can occur despite previous immune history

Slide 9 · Recognize infections by target organ

Predominant syndrome

Key source-listed pathogens

Clinical pointer

Lung

Pneumocystis; Mycobacterium tuberculosis

Pneumonia; Tuberculosis may disseminate

CNS

Cryptococcus; Toxoplasma; JC virus

Meningitis; Encephalitis/mass; PML

Eye / gut

Cytomegalovirus

Retinitis; Esophagitis; Colitis

Oral / esophageal

Candida; HSV

Candidiasis; Mucocutaneous ulcers

Intestine

Cryptosporidium; Cystoisospora; Microsporidia

Persistent watery diarrhea

Slide 10 · Pneumocystis pneumonia remains a classic AIDS complication

Pneumocystis jirovecii causes pneumonia in advanced cellular immune deficiency.

A 15–30% cumulative occurrence in untreated HIV infection.

Before effective ART, the infection was an initial manifestation in about 20% of cases.

ART responders now experience substantially less Pneumocystis pneumonia.

Slide 11 · Pneumocystis: Clinicopathologic reasoning

Falling cellular immunity

Pulmonary opportunistic infection

Respiratory presentation

Impaired CD4+ T-cell–dependent host defense

P. Jirovecii proliferates in the lung

An AIDS-associated pneumonia should prompt evaluation for this organism

Slide 12 · Candida: Oral disease as a warning sign

Candidiasis is the most common fungal infection described in AIDS by Robbins.

Common sites are the oral cavity, vagina and esophagus.

In previously asymptomatic HIV infection, oral candidiasis suggests immune deterioration.

Esophageal candidiasis is an AIDS-indicator condition in the source surveillance table.

Slide 13 · Mucosal and invasive candidiasis

Mucosal involvement

Oral, vaginal and esophageal disease predominate.

Reflects deficient mucosal host defense.

Oral involvement may signal progression.

Invasive disease

Relatively infrequent in AIDS alone.

More likely with drug-related neutropenia.

Indwelling catheters add risk.

Slide 14 · Cytomegalovirus: Severe immunosuppression

CMV can cause disseminated disease or organ-restricted eye and gastrointestinal infection.

CMV retinitis occurs almost exclusively with CD4+ T-cell counts below 50 cells/µL.

Retinitis in roughly one quarter of cases historically, with major ART-era decline.

A visual complaint in advanced AIDS raises concern for CMV retinitis.

Slide 15 · CMV disease: Retina and gastrointestinal tract

Retinal disease

Chorioretinitis / retinitis

Predominantly severe CD4+ T-cell depletion

Once frequent; Now much reduced with ART

Gastrointestinal disease

Esophagitis or colitis

Colitis may produce multiple mucosal ulcers

Reported in 5–10% of cases in source-era cohorts

Slide 16 · Mycobacterial disease: Tuberculosis versus MAC

Feature

M. Tuberculosis

M. Avium-intracellulare complex

Timing

Can appear earlier in AIDS

Usually late, marked immune deficiency

Origin

Primary infection or reactivation

Disseminated opportunistic infection

Distribution

Pulmonary or multiple organs

Systemic dissemination emphasized

Important distinction

Drug resistance is a concern

Severity reflects profound immunosuppression

Slide 17 · Tuberculosis in patients with AIDS

HIV increases susceptibility to both new tuberculosis and reactivation of latent infection.

The lung may be the only site, or infection may involve multiple organs.

Dissemination becomes more likely as CD4+ T-cell depletion worsens.

Tuberculosis as a major contributor to global AIDS deaths.

Slide 18 · TB dissemination tracks impaired cellular immunity

Tuberculosis infection

Weakening granulomatous containment

Extrapulmonary spread

Primary infection or reactivated bacilli

CD4+ T-cell dysfunction undermines localized control

Extensive disease may occur with sparse granulomatous response

Slide 19 · MAC: A late disseminated opportunistic infection

Atypical mycobacterial infection is most closely associated with advanced AIDS.

M. Avium-intracellulare complex as the principal example.

Dissemination distinguishes the usual AIDS presentation from a localized process.

A late systemic presentation should prompt consideration of severe immunodeficiency.

Slide 20 · Cryptococcus: Meningitis is the dominant syndrome

Cryptococcus neoformans is a major opportunistic fungal pathogen.

The characteristic AIDS presentation is cryptococcal meningitis.

Cryptococcosis in about 10% of historical AIDS cases.

Clinical involvement reflects failure to contain infection within the CNS.

Slide 21 · Toxoplasma: A major cause of AIDS brain masses

Toxoplasma gondii causes encephalitis in advanced HIV infection.

The source attributes approximately half of CNS mass lesions in AIDS to toxoplasmosis.

A focal CNS lesion must be distinguished from other infection and neoplasia.

The clinical problem combines immune status, neuroanatomic findings and tissue diagnosis when needed.

Slide 22 · JC virus: Progressive multifocal leukoencephalopathy

JC virus is classified as a human papovavirus in the source text.

In HIV infection it causes progressive multifocal leukoencephalopathy (PML).

PML is an important CNS opportunistic infection rather than a tumor.

Robbins locates further CNS pathology details in the nervous system chapter.

Slide 23 · CNS opportunistic infections: Syndrome recognition

Agent

Syndrome emphasized by Robbins

Distinguishing clue

Cryptococcus neoformans

Meningitis

Meningeal presentation

Toxoplasma gondii

Encephalitis / mass lesion

Focal mass-effect presentation

JC virus

PML

Progressive demyelinating syndrome

CMV

Possible CNS infection

Profound immunosuppression context

Slide 24 · Herpes simplex virus: Extensive mucosal ulcers

HSV may produce ulceration of oral and esophageal mucosa.

Genital and perianal mucocutaneous sites are also commonly involved.

Distribution can involve multiple sites in a severely immunosuppressed patient.

Persistent or atypical ulcers should be investigated for an infectious cause.

Slide 25 · Chronic watery diarrhea: Protozoal infections

Cryptosporidium and Cystoisospora belli are prominent protozoal causes.

Microsporidia are additional opportunistic intestinal pathogens.

Untreated advanced AIDS may produce profuse, persistent watery diarrhea.

Fluid loss can be substantial and makes the illness clinically consequential.

Slide 26 · Diarrhea: Protozoal versus bacterial possibilities

Protozoal / microsporidial

Cryptosporidium

Cystoisospora belli

Microsporidia

Bacterial / mycobacterial

Salmonella

Shigella

M. Avium-intracellulare

Slide 27 · Additional source-listed AIDS infections

Microbial group

Examples

AIDS-indicator manifestation

Fungal

Histoplasma; Coccidioides

Disseminated infection

Bacterial

Nocardia

Pneumonia, meningitis or disseminated disease

Bacterial

Salmonella

Disseminated infection

Viral

Varicella-zoster virus

Localized or disseminated infection

Slide 28 · AIDS surveillance infections: Category map

Group

Organisms Table 6.16

Illustrative site

Protozoa / related

Cryptosporidium; Cystoisospora; Toxoplasma; Pneumocystis

Enteritis; Brain; Lung

Fungi

Candida; Cryptococcus; Histoplasma; Coccidioides

Esophagus; CNS; Systemic

Bacteria

Mycobacteria; Nocardia; Salmonella

Systemic or focal infection

Viruses

CMV; HSV; VZV; JC virus

Retina, gut, mucosa, CNS

Slide 29 · AIDS indicators are context-specific

The source reproduces a historic CDC clinical-category framework (A, B and C).

Category C encompasses AIDS indicator infections, neoplasms and neurologic conditions.

The older source table also stratifies CD4+ T-cell categories.

This historical classification should not be presented as a verified current surveillance rule.

Slide 30 · AIDS-associated tumor biology: Three linked processes

Chronic viral infection

Loss of effective immune control

Clonal neoplastic proliferation

HHV8, EBV and oncogenic HPV can persist in hosts

Defective cell-mediated surveillance permits infected-cell expansion

Additional growth and genetic events contribute to malignancy

Slide 31 · Major AIDS-associated tumors and viral associations

Tumor / lesion

Virus emphasized

Clinicopathologic consequence

Kaposi sarcoma

HHV8 / KSHV

Vascular spindle-cell lesions

Aggressive B-cell lymphoma

EBV in a subset; HHV8 in selected types

Often extranodal

Cervical squamous carcinoma

Oncogenic HPV

Precursor squamous lesions

Anal squamous carcinoma

Oncogenic HPV

HPV-driven epithelial neoplasia

Slide 32 · Kaposi sarcoma: Characteristic epidemiology

KS is strongly associated with infection by human herpesvirus 8.

AIDS-associated disease can involve skin, mucosal surfaces and visceral organs.

The source describes a dramatic incidence decline in regions with effective ART.

KS remains prominent where HIV disease is frequent and inadequately treated.

Slide 33 · Kaposi sarcoma morphology: An interpretive checklist

Component

Source-described finding

Interpretation

Tumor cells

Proliferating spindle-shaped cells

Vascular/mesenchymal phenotype

Vascular spaces

Numerous slit-like channels

Angiogenic architecture

Inflammation

Lymphocytes and macrophages

Reactive microenvironment

Clonality

Polyclonal/oligoclonal in many lesions

Growth biology may be heterogeneous

Slide 34 · Kaposi sarcoma: A self-reinforcing microenvironment

HHV8-infected spindle cells

Angiogenic and inflammatory mediators

Recruitment and tumor-cell support

Virus-associated proliferation; Cofactors also matter

Spindle-cell secretion recruits vessels and inflammatory cells

Microenvironmental signals further support survival and growth

Slide 35 · HHV8 is necessary but not sufficient for KS

HHV8 infection causally established in Kaposi sarcoma.

Latent viral proteins may stimulate proliferation and reduce apoptosis.

Additional cofactors are required; AIDS-associated immunosuppression is important.

The precise sequence of all HHV8-dependent transforming events remains incompletely understood.

Slide 36 · Disseminated Kaposi sarcoma: Anatomic extent

Site

Expected clinical context

Teaching implication

Skin / mucosa

Visible vascular lesions

May be multisite

Gastrointestinal tract

Visceral involvement

External disease does not establish full extent

Lymph nodes

Nodal involvement

Evaluate multisystem spread

Lungs

Pulmonary involvement

Visceral presentation may dominate

Slide 37 · HHV8 also participates in B-cell disease

HHV8 can be present in the B-cell compartment, not only endothelial-lineage lesions.

Primary effusion lymphoma is an HHV8-associated neoplasm.

Multicentric Castleman disease is an HHV8-linked B-cell lymphoproliferative disorder.

The association is distinct from the vascular phenotype of KS.

Slide 38 · Lymphoma is an important AIDS-associated malignancy

Lymphomas are predominantly derived from transformed B cells.

Roughly 5% of AIDS patients present with lymphoma and another 5% develop it later.

The source estimates a markedly increased risk of aggressive B-cell lymphoma and Hodgkin lymphoma.

ART reduced incidence in some populations, but residual risk persists.

Slide 39 · Two complementary paths to HIV-associated B-cell lymphoma

Germinal center B-cell hyperplasia

Accumulation of oncogenic DNA lesions

Aggressive B-cell lymphoma

Persistent B-cell activation in HIV

Error-prone class switching / somatic hypermutation may produce translocations

Examples include MYC- or BCL6-associated lymphomas

Slide 40 · Virus-driven lymphoma: Loss of immune surveillance

Latent EBV / HHV8 in B cells

CD8+ T-cell control becomes inadequate

Expansion of virus-infected B-cell clones

Oncogenic viruses can persist without clinical lymphoma

Cell-mediated immunity ordinarily restrains proliferation

Additional mutations enable malignant outgrowth

Slide 41 · Germinal-center activation creates genetic risk

Early HIV infection may produce marked germinal-center B-cell hyperplasia.

Class-switch recombination and somatic hypermutation involve DNA damage.

Activation-induced cytidine deaminase participates in these error-prone reactions.

Aberrant oncogene/Ig-locus rearrangement can contribute to Burkitt or large B-cell lymphoma.

Slide 42 · EBV-related aggressive lymphoma in AIDS

Failure of T-cell surveillance allows EBV-infected B cells to expand.

Immune activation and cytokines, including IL-6, may support proliferation.

Successive mutations can convert proliferating clones into malignant lymphoma.

Frequent extranodal sites include CNS, gut, orbit and lung.

Slide 43 · HIV-associated lymphoma: Viral and nonviral pathways

Virus-associated tumors

EBV-positive aggressive B-cell lymphomas

HHV8-associated primary effusion lymphoma

EBV-associated Hodgkin lymphoma

Not necessarily virus-associated

Burkitt lymphoma with MYC rearrangement

Large B-cell lymphoma with BCL6 rearrangement

May arise despite preserved CD4+ T-cell counts

Slide 44 · Primary effusion lymphoma: Distinctive presentation

Primary effusion lymphoma usually presents as a malignant body-cavity effusion.

HHV8 infection is a defining viral association in the source.

Tumor cells often harbor both HHV8 and EBV.

This illustrates oncogenic cooperation between two persistent viruses.

Slide 45 · HIV-associated Hodgkin lymphoma

Hodgkin lymphoma incidence is elevated in HIV infection.

The source reports EBV within Reed–Sternberg cells in virtually all HIV-associated cases.

Low CD4+ T-cell counts are present in many, but not all, patients.

Its reactive inflammatory background contrasts with the neoplastic B-cell component.

Slide 46 · Oral hairy leukoplakia is EBV-associated

EBV can drive squamous epithelial proliferation in the oral mucosa.

The resulting white projections commonly involve the tongue.

It is distinct from Candida infection despite both appearing as oral white lesions.

Oral lesions can provide important clues to the underlying immune defect.

Slide 47 · White oral lesions: Two infectious mechanisms

Candidiasis

Fungal mucosal infection

Can signal immunologic deterioration

Oral and esophageal involvement are common

Hairy leukoplakia

EBV-driven squamous proliferation

Projections on the tongue

A virus-associated epithelial lesion

Slide 48 · HPV-associated carcinomas in HIV infection

Invasive cervical cancer and anal cancer are AIDS-associated epithelial neoplasms.

Oncogenic HPV is central to the pathogenesis of these tumors.

Immune deficiency weakens control of HPV-infected epithelial cells.

Clinical consequences include precursor lesions and invasive carcinoma.

Slide 49 · HIV–HPV interaction: Epithelial neoplasia risk

Persistent oncogenic HPV

Deficient immune surveillance

Squamous precursor lesion → carcinoma

Persistent virus-infected squamous epithelium

Lower CD4+ T-cell counts correlate with elevated lesion frequency

Progression risk can be accelerated in HIV infection

Slide 50 · Cervical squamous intraepithelial lesions

Increased frequency of cervical squamous intraepithelial lesions in HIV-infected females.

Precursor lesions are especially prevalent in women with lower CD4+ T-cell counts.

The source describes accelerated progression from precursor lesion to carcinoma.

Gynecologic examination is therefore emphasized in routine care.

Slide 51 · AIDS-associated tumors: Practical distinction

Disease

Primary tissue phenotype

Pathogenetic association

Kaposi sarcoma

Spindle-cell / vascular proliferation

HHV8, plus host cofactors

B-cell lymphoma

Lymphoid neoplasm

B-cell hyperplasia ± EBV/HHV8

Cervical cancer

Squamous epithelial malignancy

Oncogenic HPV

Anal cancer

Squamous epithelial malignancy

Oncogenic HPV

Slide 52 · Neurologic involvement may be the earliest clinical clue

Neurologic disease is common in advanced HIV infection.

Neurologic manifestations can precede recognition of the underlying infection.

The source reports substantial clinical and autopsy involvement in historical AIDS cohorts.

The differential includes direct HIV-related injury, infections and neoplasms.

Slide 53 · CNS disease: Major mechanistic categories

Category

Examples

Clinical implication

Direct / immune-mediated

HIV-associated neurocognitive disorder

Progressive cognitive dysfunction

Opportunistic infection

Cryptococcus; Toxoplasma; JC virus

Meningitis; Mass lesion; PML

Neoplasm

Primary CNS lymphoma

Space-occupying disease

Other HIV-associated

Aseptic meningitis; Myelopathy; Neuropathy

Diverse neurologic syndromes

Slide 54 · HIV-associated neurocognitive disorder

HIV-infected microglial compartment

Local immune response in CNS

Progressive encephalopathy

Brain-resident myeloid lineage is implicated

Neuroinflammation can amplify damage

Cognitive impairment may be a major clinical manifestation

Slide 55 · Additional HIV-related neurologic manifestations

A self-limited meningoencephalitis may accompany early seroconversion.

Aseptic meningitis is another recognized HIV-related manifestation.

Vacuolar myelopathy and peripheral neuropathies broaden the neurologic spectrum.

Opportunistic CNS infections and neoplasms remain distinct diagnostic categories.

Slide 56 · AIDS morphology is not individually pathognomonic

Opportunistic infections, Kaposi sarcoma and B-cell lymphoma dominate pathologic findings.

None of these lesions by itself is uniquely restricted to HIV infection.

The immune status and pattern of concurrent lesions are clinically informative.

Robbins refers detailed organ-specific pathology to other chapters.

Slide 57 · Lymph node evolution: Early versus advanced HIV

Early lymph node

Marked B-cell follicular hyperplasia

Large, irregular or serpiginous germinal centers

Thinned mantle zones and expanded follicles

Late lymph node

Severe lymphoid depletion and involution

Disrupted follicular dendritic-cell network

Hyalinized germinal centers / atrophic nodes

Slide 58 · Early lymphadenopathy reflects polyclonal B-cell activation

Chronic antigenic stimulation

Germinal-center hyperplasia

Enlarged lymph nodes

HIV-associated immune dysregulation stimulates B cells

Prominent follicles can impinge on T-cell regions

Morphology mirrors clinical generalized lymphadenopathy

Slide 59 · Late lymphoid involution: Loss of immune architecture

Progression may replace follicular hyperplasia with marked tissue atrophy.

FDC networks become disorganized, and germinal centers may be hyalinized.

Lymph nodes may contain opportunistic organisms within macrophages.

Spleen and thymus may also become severely lymphocyte-depleted.

Slide 60 · In advanced AIDS, inflammation can be deceptively sparse

Profound CD4+ T-cell deficiency alters the expected tissue response to infection.

Mycobacteria may fail to produce well-formed granulomas.

Lymph nodes and involved organs may appear unexpectedly hypocellular.

Special stains can be necessary to demonstrate microorganisms.

Slide 61 · Mycobacterial infection: Differing tissue reactions

Immune-competent setting

Activated cell-mediated response

Granulomatous inflammation can contain bacilli

Organized host reaction is often recognizable

Advanced AIDS

Deficient CD4+ T-cell response

Granulomas may be poorly formed or absent

High organism burden may be subtle on routine stains

Slide 62 · How ART reverses the AIDS trajectory

Suppress viral replication

Halt progressive CD4+ T-cell loss

Gradual immune recovery

Multidrug regimens interrupt different HIV lifecycle steps

Sustained viral control limits further immunologic injury

Peripheral CD4+ T-cell counts may rise over years

Slide 63 · ART reduces classic AIDS morbidity

Effective regimens combine active drugs to limit emergence of resistance.

The source describes durable viral suppression while effective treatment continues.

Pneumocystis disease and Kaposi sarcoma became much less frequent in effectively treated populations.

Prevention of HIV transmission is an additional public-health benefit.

Slide 64 · Viral suppression is not eradication

HIV DNA persists within lymphoid tissues despite successful treatment.

A sustained undetectable plasma viral load does not establish virologic cure.

The source notes viral rebound after treatment discontinuation.

Persistent reservoirs are a fundamental reason long-term management remains necessary.

Slide 65 · Immune reconstitution inflammatory syndrome (IRIS)

Severe immune depletion before ART

ART-induced immune restoration

Inflammatory clinical deterioration

High residual burden of microbial antigens can persist

CD4+ counts rise as viral load declines

Dysregulated immune responses can reveal or exacerbate inflammatory illness

Slide 66 · IRIS: Identify the paradox

Clinical worsening can occur after ART is started in patients with advanced immunosuppression.

This may coincide with rising CD4+ T cells and falling HIV viral load.

Excessive response to persistent microbial antigens.

Deterioration alone should not automatically be interpreted as ART virologic failure.

Slide 67 · Long-term ART: Adverse effects in the source

Domain

Examples listed by Robbins

Clinical consequence

Adipose distribution

Lipoatrophy; Central fat accumulation

Altered body fat phenotype

Metabolic

Dyslipidemia; Insulin resistance

Metabolic risk

Neurologic

Peripheral neuropathy

Nervous system morbidity

Organ toxicity

Cardiac, renal and hepatic effects

Long-term monitoring concerns

Slide 68 · Non-AIDS morbidity becomes prominent with longer survival

Effective ART extends survival and frequently restores peripheral CD4+ T-cell counts.

Cancer and cardiovascular, kidney and liver disease become important morbidity drivers.

The mechanisms are incompletely understood in the source.

Persistent inflammation and residual immune dysfunction are proposed contributors.

Slide 69 · Clinical reasoning: Progression versus immune recovery

Uncontrolled HIV / AIDS progression

Falling CD4+ T-cell counts

Opportunistic infection or neoplasm

Uncontrolled or increasing HIV replication

Immune restoration with IRIS

ART-associated falling viral load

Rising CD4+ T-cell counts

Inflammatory exacerbation despite virologic improvement

Slide 70 · Case: Fever, weight loss and chronic diarrhea

A patient with advanced, untreated HIV has weight loss, persistent fever, and profuse watery diarrhea.

Organism groups to consider

Cryptosporidium or Cystoisospora

Microsporidia; Enteric bacteria

Disseminated mycobacterial infection

Slide 71 · Case: Focal brain lesion in advanced AIDS

A patient with advanced HIV infection develops a focal neurologic syndrome and a brain mass lesion.

Source-based major considerations

Toxoplasma encephalitis

Primary CNS lymphoma

Other causes require independent assessment

Slide 72 · Case: Oral white lesion

A person with HIV develops a white lesion on the tongue; The source provides two biologically distinct causes.

Differential to articulate

Candida-associated mucosal infection

EBV-driven oral hairy leukoplakia

Site, morphology and tests help distinguish them

Slide 73 · Case: Lymph node biopsy

An enlarged node in an earlier HIV phase shows exuberant large follicles; In a later phase another biopsy is hypocellular.

Expected interpretation

Early: Polyclonal B-cell stimulation

Late: Lymphoid involution and FDC damage

Late opportunists may need special stains

Slide 74 · Syndrome-to-pathogen review

Presentation

Important association

Underlying theme

Pneumonia

Pneumocystis jirovecii

Compromised cellular immunity

Retinitis

Cytomegalovirus

Very low CD4+ counts

Meningitis

Cryptococcus neoformans

CNS opportunistic fungus

Focal CNS mass

Toxoplasma; Lymphoma differential

Opportunism or neoplasia

Visceral vascular lesions

Kaposi sarcoma / HHV8

Impaired tumor-virus surveillance

Slide 75 · Integrated clinical conclusions

AIDS manifests as progressive immune failure with infections, selected neoplasms and neurologic syndromes.

Site and tempo help prioritize infectious differential diagnoses.

HHV8, EBV and HPV link deficient viral immune surveillance to malignancy.

ART alters the disease spectrum but does not eliminate viral reservoirs or chronic morbidity.

Slide 76 · Reference and interpretive limits

Primary source: Robbins, Cotran & Kumar, Pathologic Basis of Disease, 11th ed., Chapter 6, pp. 226–230.

Context: preceding “Natural History of HIV Infection” section, pp. 224–226.

The clinical frequency estimates reflect the cohorts and treatment context cited in that edition.

This pathology lecture is not a current HIV treatment or surveillance manual.