Questions

Viral Infections in Acquired Immunodeficiency Syndrome — Questions

Study questions for Viral Infections in Acquired Immunodeficiency Syndrome.

Mock Exam mode

Sit this set one question at a time. Multiple-choice questions mark themselves; written questions reveal a tickable mark scheme so you can score your own answer. You get a combined score at the end.

15 questions: 11 MCQ, 4 written.

High-priority (past-paper) questions only

Why E

Cytomegalovirus end-organ disease, retinitis above all, is the classic very-late opportunistic infection, appearing below a CD4 count of about 50 cells per microlitre. It marks the deepest immunosuppression on the CD4 ladder.

The higher counts correspond to earlier events: zoster and more severe herpes simplex below 350, the AIDS threshold and disseminated zoster below 200, and chronic herpes simplex, the EBV-driven systemic lymphomas and progressive multifocal leukoencephalopathy below 100. Cytomegalovirus, with primary central nervous system lymphoma, sits at the bottom, below 50.

Why B

CMV retinitis produces well-demarcated areas of full-thickness retinal necrosis, seen as fluffy or granular white opacification that spreads along the retinal vessels and is accompanied by retinal haemorrhages. Characteristically there is little vitreous inflammation, because the CD4 count is so low that the eye mounts only a weak inflammatory response, which is why prominent vitreous inflammation argues against the diagnosis.

A swollen disc, isolated cotton-wool spots, and a macular cherry-red spot point to other diagnoses. The appearance is characteristic enough that retinitis is diagnosed clinically on dilated fundoscopy by an experienced examiner.

Why B

Kaposi sarcoma is driven by human herpesvirus 8 under failing immune control, and antiretroviral therapy is first-line for limited cutaneous disease: restoring immunity often causes the lesions to regress without specific cancer treatment.

Systemic chemotherapy such as liposomal doxorubicin or paclitaxel is reserved for advanced, visceral or rapidly progressive disease, given alongside antiretroviral therapy. Surgery and radiotherapy have only local roles, and antivirals such as ganciclovir are of unproven benefit.

Why D

There is no specific antiviral for the JC virus. The only effective intervention is antiretroviral therapy, which restores CD4 immunity and lets the patient regain control of the virus; immune reconstitution is the principal determinant of survival, and antiretroviral therapy should not be delayed.

Ganciclovir, aciclovir and cidofovir have no useful activity against JC virus. Corticosteroids are used only to dampen a severe immune-reconstitution reaction (PML-IRIS), not as primary treatment, and the outlook remains poor even with antiretroviral therapy.

Why C

HIV depletes CD4 T lymphocytes, and with them the cell-mediated immunity that controls intracellular and latent viruses. The herpesviruses, the JC polyomavirus and the oncogenic viruses are all held in check by CD4-dependent T-cell responses, so as the CD4 count falls they reactivate and cause disease.

The other options are not the principal defect: antibody, complement and neutrophil function are relatively preserved (B-cell responses are in fact hyperactivated), and it is the loss of T-cell help, not humoral or innate effectors, that opens the door to the viral opportunistic infections.

Why B

As immunity recovers on antiretroviral therapy, cytomegalovirus can drive an immune-recovery uveitis or retinitis that threatens vision even while the systemic infection improves. The other important viral causes of immune reconstitution inflammatory syndrome are JC virus (PML-IRIS, sometimes fulminant) and HHV-8 (a Kaposi-sarcoma flare), and zoster commonly appears in the early weeks of therapy.

The remaining options are acute, self-limiting infections (hepatitis A, rhinovirus, rotavirus, norovirus) that are not associated with immune reconstitution inflammatory syndrome.

A complete answer recognises the likely diagnosis, confirms it, treats it, and anticipates the complication of immune recovery.

Recognise the diagnosis

At a CD4 count of 30, floaters and reduced acuity are CMV retinitis until proven otherwise: it is the commonest end-organ cytomegalovirus disease and appears at this depth of immunosuppression. Sight near the macula or optic disc is immediately at risk.

Confirm it

The diagnosis is clinical, made on dilated fundoscopy by an experienced examiner, who looks for well-demarcated full-thickness retinal necrosis with fluffy white opacification along the vessels and accompanying haemorrhage, with little vitritis. A blood cytomegalovirus PCR supports the diagnosis and gives a baseline to follow, though it can be low in eye-limited disease. The diagnosis remains clinical, but where the appearance is atypical or a similar infection must be excluded (such as herpes simplex or varicella-zoster retinal necrosis, toxoplasma chorioretinitis or syphilis), PCR on an intraocular (aqueous or vitreous) sample can establish the cause.

Treat it

Start systemic valganciclovir or ganciclovir as induction then maintenance until immune recovery (a sustained CD4 count above 100), with intravitreal therapy for immediately sight-threatening lesions and foscarnet or cidofovir as alternatives. Antiretroviral therapy is essential, since durable control depends on restoring immunity.

Anticipate immune recovery

Warn of, and watch for, immune-recovery uveitis, a form of immune reconstitution inflammatory syndrome in which the recovering response inflames the eye and can itself threaten vision; it is managed with corticosteroids while both antiretroviral and anti-cytomegalovirus therapy continue.

A complete answer states the principle and then works down the CD4 strata with examples.

The principle

As the CD4 count falls, cell-mediated control of the latent viruses fails in a predictable sequence, so the count both anticipates which infection to expect and frames how aggressively to treat and monitor. AIDS is defined by a CD4 count below 200 cells per microlitre or an AIDS-defining condition.

The ladder

Below 350: herpes zoster, and more frequent and severe mucocutaneous herpes simplex.
Below 200: multidermatomal or disseminated zoster; oral hairy leukoplakia.
Below 100: chronic or visceral herpes simplex; EBV-driven systemic non-Hodgkin lymphoma; progressive multifocal leukoencephalopathy (JC virus).
Below 50: cytomegalovirus end-organ disease (retinitis, colitis); EBV primary central nervous system lymphoma.

Outside the ladder

Kaposi sarcoma (HHV-8) and HPV-related cancers occur across a range of counts, and hepatitis B is governed by coinfection rather than a threshold. The thresholds are a guide, and disease can present outside its usual band.

A complete answer covers the three viral drivers, the tumours each causes, and the central role of antiretroviral therapy.

Kaposi sarcoma (HHV-8)

Human herpesvirus 8 causes Kaposi sarcoma, violaceous skin and mucosal lesions (characteristically the palate and gingiva) that can involve the gut and lungs, and also primary effusion lymphoma and multicentric Castleman disease. Antiretroviral therapy is first-line for limited disease, with chemotherapy for advanced or visceral disease.

The AIDS lymphomas (EBV)

Epstein-Barr virus drives the AIDS-defining lymphomas: systemic non-Hodgkin lymphoma (diffuse large B-cell, Burkitt and plasmablastic types) and primary central nervous system lymphoma, which is almost always EBV-positive and is distinguished from cerebral toxoplasmosis by EBV DNA in the cerebrospinal fluid and by metabolic imaging. Treatment combines chemotherapy, often with rituximab for systemic disease and high-dose methotrexate for central nervous system disease, with antiretroviral therapy.

Cervical and anal cancer (HPV)

Human papillomavirus causes accelerated cervical and anal intraepithelial neoplasia and a several-fold higher risk of invasive cervical cancer (an AIDS-defining condition) and anal cancer, which is why regular cervical and anal screening is essential.

The common thread

All three are controlled by cell-mediated immunity, so antiretroviral therapy underpins management of each, with tumour-specific treatment added according to the malignancy.

A complete answer explains the immune defect, why it matters for these particular viruses, and the CD4-strata pattern of disease.

The immune defect

HIV infects and depletes CD4 T lymphocytes through several mechanisms acting together: direct killing of infected cells, syncytium formation, and, most importantly, the chronic immune activation that follows early depletion of CD4 cells from gut-associated lymphoid tissue and the resulting microbial translocation. The CD8 cytotoxic T cells that initially control the virus become exhausted. The result is progressive failure of cell-mediated immunity.

Why these viruses

Cell-mediated immunity is exactly the arm that contains the latent herpesviruses, the JC polyomavirus and the oncogenic viruses. As it fails, these viruses reactivate and cause disease, whereas antibody-controlled infections are comparatively spared.

The CD4-strata pattern

Disease appears in a predictable order as the count falls: zoster and more severe herpes simplex below 350; disseminated zoster and oral hairy leukoplakia below 200 (the AIDS threshold); chronic or visceral herpes simplex, EBV-driven systemic lymphoma and progressive multifocal leukoencephalopathy below 100; and cytomegalovirus end-organ disease with primary central nervous system lymphoma below 50. Kaposi sarcoma and HPV-related cancers occur across a range of counts.

The implication for management

Because the defect is loss of CD4 immunity, antiretroviral therapy is the single most effective measure: restoring the CD4 count reverses the susceptibility, and specific antivirals are added only for the infections that need them.

Why E

Failure to heal on adequate aciclovir suggests aciclovir resistance, which arises through viral thymidine-kinase mutations with prolonged exposure. Because resistant virus cannot activate aciclovir, valaciclovir or famciclovir (all of which depend on the same kinase), the answer is to switch to foscarnet, which acts directly on the viral polymerase and needs no activation.

Raising the aciclovir dose or changing to another thymidine-kinase-dependent drug will not work against a resistant strain, a corticosteroid does not treat the infection, and ganciclovir shares the activation problem. A chronic herpes simplex ulcer persisting beyond a month is itself an AIDS-defining condition.

Reactivation of varicella-zoster as shingles occurs at a relatively high CD4 count and is often the first clue to undiagnosed HIV in a young adult, so it should prompt HIV testing. As immunity falls further, zoster becomes multidermatomal or disseminated and can cause encephalitis, a retinal necrosis and a stroke-causing vasculopathy.

Reassurance alone misses an opportunity to diagnose HIV, lifelong suppression is not indicated for a single episode, a live vaccine is inappropriate when immunodeficiency is suspected, and a clotting screen is irrelevant.

Why A

Oral hairy leukoplakia is an Epstein-Barr virus lesion: corrugated white plaques on the lateral border of the tongue that do not rub off. It is harmless but a useful clinical marker of immunosuppression, and it needs no specific treatment, regressing with immune recovery on antiretroviral therapy.

Herpes simplex, cytomegalovirus and human papillomavirus do not cause it, and Candida (a distractor because oral candidiasis is also common in HIV) wipes off and is fungal, not the cause of the adherent plaques of hairy leukoplakia.

Why A

Unlike the non-viral opportunistic infections, where co-trimoxazole prophylaxis is standard, the viral infections are not prevented by routine antiviral prophylaxis. For cytomegalovirus the approach is early antiretroviral therapy, patient education (prompt reporting of visual symptoms) and targeted ophthalmological review at the lowest counts, rather than giving an antiviral to everyone.

Routine valganciclovir or letermovir prophylaxis, immunoglobulin and prophylactic intravitreal therapy are not recommended: they carry toxicity, cost and resistance without a survival benefit, and restoring immunity with antiretroviral therapy is what removes the risk.

Why C

Primary central nervous system lymphoma is almost always EBV-positive, so EBV DNA in the cerebrospinal fluid points to lymphoma rather than toxoplasmosis. Metabolic imaging helps in the same way (the lymphoma is hypermetabolic on positron emission tomography or thallium scanning, whereas toxoplasmosis is not), and brain biopsy resolves remaining doubt.

The other features do not separate the two: both occur at low CD4 counts, both cause focal deficits and constitutional symptoms, and both can appear as enhancing or ring-enhancing mass lesions on imaging.

High priorityMCQ
Cytomegalovirus end-organ disease in AIDS characteristically appears below which CD4 count?
- A. 500 cells per microlitre
- B. 350 cells per microlitre
- C. 200 cells per microlitre
- D. 100 cells per microlitre
- E. 50 cells per microlitre
Show answer
Correct answer: E
Why E

Cytomegalovirus end-organ disease, retinitis above all, is the classic very-late opportunistic infection, appearing below a CD4 count of about 50 cells per microlitre. It marks the deepest immunosuppression on the CD4 ladder.

The higher counts correspond to earlier events: zoster and more severe herpes simplex below 350, the AIDS threshold and disseminated zoster below 200, and chronic herpes simplex, the EBV-driven systemic lymphomas and progressive multifocal leukoencephalopathy below 100. Cytomegalovirus, with primary central nervous system lymphoma, sits at the bottom, below 50.
High priorityMCQ
What is the characteristic fundoscopic appearance of CMV retinitis in AIDS?
- A. A pale, swollen optic disc
- B. Retinal necrosis with haemorrhage
- C. Dense vitritis obscuring the retina
- D. Scattered cotton-wool spots alone
- E. A cherry-red spot at the macula
Show answer
Correct answer: B
Why B

CMV retinitis produces well-demarcated areas of full-thickness retinal necrosis, seen as fluffy or granular white opacification that spreads along the retinal vessels and is accompanied by retinal haemorrhages. Characteristically there is little vitreous inflammation, because the CD4 count is so low that the eye mounts only a weak inflammatory response, which is why prominent vitreous inflammation argues against the diagnosis.

A swollen disc, isolated cotton-wool spots, and a macular cherry-red spot point to other diagnoses. The appearance is characteristic enough that retinitis is diagnosed clinically on dilated fundoscopy by an experienced examiner.
High priorityMCQ
What is the first-line treatment for limited cutaneous Kaposi sarcoma in a patient with HIV?
- A. Liposomal doxorubicin
- B. Antiretroviral therapy
- C. Wide surgical excision
- D. Radiotherapy to each lesion
- E. Ganciclovir
Show answer
Correct answer: B
Why B

Kaposi sarcoma is driven by human herpesvirus 8 under failing immune control, and antiretroviral therapy is first-line for limited cutaneous disease: restoring immunity often causes the lesions to regress without specific cancer treatment.

Systemic chemotherapy such as liposomal doxorubicin or paclitaxel is reserved for advanced, visceral or rapidly progressive disease, given alongside antiretroviral therapy. Surgery and radiotherapy have only local roles, and antivirals such as ganciclovir are of unproven benefit.
High priorityMCQ
What is the most effective treatment for progressive multifocal leukoencephalopathy in a patient with AIDS?
- A. Intravenous ganciclovir
- B. High-dose aciclovir
- C. Cidofovir
- D. Antiretroviral therapy
- E. Corticosteroids alone
Show answer
Correct answer: D
Why D

There is no specific antiviral for the JC virus. The only effective intervention is antiretroviral therapy, which restores CD4 immunity and lets the patient regain control of the virus; immune reconstitution is the principal determinant of survival, and antiretroviral therapy should not be delayed.

Ganciclovir, aciclovir and cidofovir have no useful activity against JC virus. Corticosteroids are used only to dampen a severe immune-reconstitution reaction (PML-IRIS), not as primary treatment, and the outlook remains poor even with antiretroviral therapy.
High priorityMCQ
Which arm of the immune response, lost in advanced HIV, accounts for the viral opportunistic infections of AIDS?
- A. Mucosal IgA secretion
- B. The complement cascade
- C. CD4 cell-mediated immunity
- D. Neutrophil phagocytosis
- E. Pre-formed neutralising antibody
Show answer
Correct answer: C
Why C

HIV depletes CD4 T lymphocytes, and with them the cell-mediated immunity that controls intracellular and latent viruses. The herpesviruses, the JC polyomavirus and the oncogenic viruses are all held in check by CD4-dependent T-cell responses, so as the CD4 count falls they reactivate and cause disease.

The other options are not the principal defect: antibody, complement and neutrophil function are relatively preserved (B-cell responses are in fact hyperactivated), and it is the loss of T-cell help, not humoral or innate effectors, that opens the door to the viral opportunistic infections.
High priorityMCQ
Which virus is a recognised cause of immune reconstitution inflammatory syndrome after antiretroviral therapy is started?
- A. Hepatitis A virus
- B. Cytomegalovirus
- C. Rhinovirus
- D. Rotavirus
- E. Norovirus
Show answer
Correct answer: B
Why B

As immunity recovers on antiretroviral therapy, cytomegalovirus can drive an immune-recovery uveitis or retinitis that threatens vision even while the systemic infection improves. The other important viral causes of immune reconstitution inflammatory syndrome are JC virus (PML-IRIS, sometimes fulminant) and HHV-8 (a Kaposi-sarcoma flare), and zoster commonly appears in the early weeks of therapy.

The remaining options are acute, self-limiting infections (hepatitis A, rhinovirus, rotavirus, norovirus) that are not associated with immune reconstitution inflammatory syndrome.
High priorityClinical scenarioA patient with AIDS and a CD4 count of 30 cells per microlitre reports floaters and reduced vision in one eye. Discuss your approach to diagnosis and management. [10]
Model answer
A complete answer recognises the likely diagnosis, confirms it, treats it, and anticipates the complication of immune recovery.

Recognise the diagnosis

At a CD4 count of 30, floaters and reduced acuity are CMV retinitis until proven otherwise: it is the commonest end-organ cytomegalovirus disease and appears at this depth of immunosuppression. Sight near the macula or optic disc is immediately at risk.

Confirm it

The diagnosis is clinical, made on dilated fundoscopy by an experienced examiner, who looks for well-demarcated full-thickness retinal necrosis with fluffy white opacification along the vessels and accompanying haemorrhage, with little vitritis. A blood cytomegalovirus PCR supports the diagnosis and gives a baseline to follow, though it can be low in eye-limited disease. The diagnosis remains clinical, but where the appearance is atypical or a similar infection must be excluded (such as herpes simplex or varicella-zoster retinal necrosis, toxoplasma chorioretinitis or syphilis), PCR on an intraocular (aqueous or vitreous) sample can establish the cause.

Treat it

Start systemic valganciclovir or ganciclovir as induction then maintenance until immune recovery (a sustained CD4 count above 100), with intravitreal therapy for immediately sight-threatening lesions and foscarnet or cidofovir as alternatives. Antiretroviral therapy is essential, since durable control depends on restoring immunity.

Anticipate immune recovery

Warn of, and watch for, immune-recovery uveitis, a form of immune reconstitution inflammatory syndrome in which the recovering response inflames the eye and can itself threaten vision; it is managed with corticosteroids while both antiretroviral and anti-cytomegalovirus therapy continue.
High priorityExam-styleDescribe how the CD4 count predicts the viral opportunistic infections seen in HIV. [5]
Model answer
A complete answer states the principle and then works down the CD4 strata with examples.

The principle

As the CD4 count falls, cell-mediated control of the latent viruses fails in a predictable sequence, so the count both anticipates which infection to expect and frames how aggressively to treat and monitor. AIDS is defined by a CD4 count below 200 cells per microlitre or an AIDS-defining condition.

The ladder
- Below 350: herpes zoster, and more frequent and severe mucocutaneous herpes simplex.
- Below 200: multidermatomal or disseminated zoster; oral hairy leukoplakia.
- Below 100: chronic or visceral herpes simplex; EBV-driven systemic non-Hodgkin lymphoma; progressive multifocal leukoencephalopathy (JC virus).
- Below 50: cytomegalovirus end-organ disease (retinitis, colitis); EBV primary central nervous system lymphoma.
Outside the ladder

Kaposi sarcoma (HHV-8) and HPV-related cancers occur across a range of counts, and hepatitis B is governed by coinfection rather than a threshold. The thresholds are a guide, and disease can present outside its usual band.
High priorityExam-styleDiscuss the virus-associated malignancies seen in AIDS. [8]
Model answer
A complete answer covers the three viral drivers, the tumours each causes, and the central role of antiretroviral therapy.

Kaposi sarcoma (HHV-8)

Human herpesvirus 8 causes Kaposi sarcoma, violaceous skin and mucosal lesions (characteristically the palate and gingiva) that can involve the gut and lungs, and also primary effusion lymphoma and multicentric Castleman disease. Antiretroviral therapy is first-line for limited disease, with chemotherapy for advanced or visceral disease.

The AIDS lymphomas (EBV)

Epstein-Barr virus drives the AIDS-defining lymphomas: systemic non-Hodgkin lymphoma (diffuse large B-cell, Burkitt and plasmablastic types) and primary central nervous system lymphoma, which is almost always EBV-positive and is distinguished from cerebral toxoplasmosis by EBV DNA in the cerebrospinal fluid and by metabolic imaging. Treatment combines chemotherapy, often with rituximab for systemic disease and high-dose methotrexate for central nervous system disease, with antiretroviral therapy.

Cervical and anal cancer (HPV)

Human papillomavirus causes accelerated cervical and anal intraepithelial neoplasia and a several-fold higher risk of invasive cervical cancer (an AIDS-defining condition) and anal cancer, which is why regular cervical and anal screening is essential.

The common thread

All three are controlled by cell-mediated immunity, so antiretroviral therapy underpins management of each, with tumour-specific treatment added according to the malignancy.
High priorityExam-styleExplain how advanced HIV predisposes to viral opportunistic infection, and outline the viral infections seen at different CD4 strata. [10]
Model answer
A complete answer explains the immune defect, why it matters for these particular viruses, and the CD4-strata pattern of disease.

The immune defect

HIV infects and depletes CD4 T lymphocytes through several mechanisms acting together: direct killing of infected cells, syncytium formation, and, most importantly, the chronic immune activation that follows early depletion of CD4 cells from gut-associated lymphoid tissue and the resulting microbial translocation. The CD8 cytotoxic T cells that initially control the virus become exhausted. The result is progressive failure of cell-mediated immunity.

Why these viruses

Cell-mediated immunity is exactly the arm that contains the latent herpesviruses, the JC polyomavirus and the oncogenic viruses. As it fails, these viruses reactivate and cause disease, whereas antibody-controlled infections are comparatively spared.

The CD4-strata pattern

Disease appears in a predictable order as the count falls: zoster and more severe herpes simplex below 350; disseminated zoster and oral hairy leukoplakia below 200 (the AIDS threshold); chronic or visceral herpes simplex, EBV-driven systemic lymphoma and progressive multifocal leukoencephalopathy below 100; and cytomegalovirus end-organ disease with primary central nervous system lymphoma below 50. Kaposi sarcoma and HPV-related cancers occur across a range of counts.

The implication for management

Because the defect is loss of CD4 immunity, antiretroviral therapy is the single most effective measure: restoring the CD4 count reverses the susceptibility, and specific antivirals are added only for the infections that need them.
MCQ
A patient with AIDS has a herpes simplex ulcer that fails to heal despite adequate aciclovir. What is the best next step?
- A. Double the aciclovir dose
- B. Change to oral valaciclovir
- C. Add a topical corticosteroid
- D. Switch to ganciclovir
- E. Switch to foscarnet
Show answer
Correct answer: E
Why E

Failure to heal on adequate aciclovir suggests aciclovir resistance, which arises through viral thymidine-kinase mutations with prolonged exposure. Because resistant virus cannot activate aciclovir, valaciclovir or famciclovir (all of which depend on the same kinase), the answer is to switch to foscarnet, which acts directly on the viral polymerase and needs no activation.

Raising the aciclovir dose or changing to another thymidine-kinase-dependent drug will not work against a resistant strain, a corticosteroid does not treat the infection, and ganciclovir shares the activation problem. A chronic herpes simplex ulcer persisting beyond a month is itself an AIDS-defining condition.
MCQ
Herpes zoster in an otherwise healthy young adult should most importantly prompt which action?
- A. Reassurance and discharge
- B. Lifelong aciclovir suppression
- C. Live zoster vaccination
- D. Testing for HIV
- E. A clotting screen
Show answer
Correct answer: D
Reactivation of varicella-zoster as shingles occurs at a relatively high CD4 count and is often the first clue to undiagnosed HIV in a young adult, so it should prompt HIV testing. As immunity falls further, zoster becomes multidermatomal or disseminated and can cause encephalitis, a retinal necrosis and a stroke-causing vasculopathy.

Reassurance alone misses an opportunity to diagnose HIV, lifelong suppression is not indicated for a single episode, a live vaccine is inappropriate when immunodeficiency is suspected, and a clotting screen is irrelevant.
MCQ
Oral hairy leukoplakia in a patient with HIV is caused by which virus?
- A. Epstein-Barr virus
- B. Herpes simplex virus
- C. Human papillomavirus
- D. Cytomegalovirus
- E. Candida albicans
Show answer
Correct answer: A
Why A

Oral hairy leukoplakia is an Epstein-Barr virus lesion: corrugated white plaques on the lateral border of the tongue that do not rub off. It is harmless but a useful clinical marker of immunosuppression, and it needs no specific treatment, regressing with immune recovery on antiretroviral therapy.

Herpes simplex, cytomegalovirus and human papillomavirus do not cause it, and Candida (a distractor because oral candidiasis is also common in HIV) wipes off and is fungal, not the cause of the adherent plaques of hairy leukoplakia.
MCQ
What is the recommended approach to preventing CMV disease in a patient with HIV and a CD4 count below 50?
- A. Education and monitoring
- B. Routine valganciclovir prophylaxis
- C. Routine letermovir prophylaxis
- D. Monthly CMV immunoglobulin
- E. Prophylactic intravitreal ganciclovir
Show answer
Correct answer: A
Why A

Unlike the non-viral opportunistic infections, where co-trimoxazole prophylaxis is standard, the viral infections are not prevented by routine antiviral prophylaxis. For cytomegalovirus the approach is early antiretroviral therapy, patient education (prompt reporting of visual symptoms) and targeted ophthalmological review at the lowest counts, rather than giving an antiviral to everyone.

Routine valganciclovir or letermovir prophylaxis, immunoglobulin and prophylactic intravitreal therapy are not recommended: they carry toxicity, cost and resistance without a survival benefit, and restoring immunity with antiretroviral therapy is what removes the risk.
MCQ
Which finding best distinguishes primary central nervous system lymphoma from cerebral toxoplasmosis in AIDS?
- A. Multiple ring-enhancing lesions on imaging
- B. A low CD4 count
- C. EBV DNA in cerebrospinal fluid
- D. Focal neurological deficits
- E. Headache and fever
Show answer
Correct answer: C
Why C

Primary central nervous system lymphoma is almost always EBV-positive, so EBV DNA in the cerebrospinal fluid points to lymphoma rather than toxoplasmosis. Metabolic imaging helps in the same way (the lymphoma is hypermetabolic on positron emission tomography or thallium scanning, whereas toxoplasmosis is not), and brain biopsy resolves remaining doubt.

The other features do not separate the two: both occur at low CD4 counts, both cause focal deficits and constitutional symptoms, and both can appear as enhancing or ring-enhancing mass lesions on imaging.