A 50-year-old African American man with HIV infection had a CD4+ T-cell count of 18/μL (1%), CD8+ cell count of 1035/μL (69%), and CD4:CD8 ratio of 0.01 at the time of diagnosis. He had multiple erythematosquamous skin lesions over his forehead, face, chest, back, and extremities

In 2006, the CDC recommended “opt-out” routine HIV testing in all health care encounters for persons 13 to 64 years of age. While this recommendation has garnered some support, concerns about the feasibility of such routine testing in a busy office without disrupting patient care has persisted. We report the results of a pilot study to determine the feasibility of routine testing in a busy urban clinic.

A 33-year-old man from the Ivory Coast (who had been living in the United States for the past 8 years) received a diagnosis of AIDS when he presented with Pneumocystis jiroveci pneumonia. His CD4+ cell count was 6/uL, and his HIV RNA level was 575,000 copies/mL. He also presented with altered sensorium and seizure activity and was found to have obstructive hydrocephalus and ring-enhancing lesions in both cerebellar hemispheres and basal ganglia. Results of polymerase chain reaction testing of cerebrospinal fluid for Toxoplasma gondii were positive, and treatment for toxoplasmosis was started. A ventricular-peritoneal shunt was placed.

Bilateral retrobulbar optic neuritis developed in a 38-year-old woman with advanced HIV infection. This was secondary to varicella-zoster virus (VZV) infection, confirmed by polymerase chain reaction detection of VZV in the patient's cerebrospinal fluid. There was no evidence of retinitis, and the ocular symptoms preceded the rash. This case illustrates that a new onset of unexplained visual loss resulting from optic neuritis in an HIV-positive patient may be caused by VZV infection. Clinicians should be aware of this unusual manifestation of VZV infection. Prompt recognition and early intervention with antivirals are needed, but it is unclear how much vision can be preserved.

We report 4 cases of bladder cancer in an ethnically diverse population of about 2500 HIV-infected patients. These patients were younger than the median age at diagnosis of bladder cancer in the United States.

London-based GlaxoSmithKline (GSK) plc and New York–based Pfizer Inc have announced they will combine their HIV drug divisions into a new company (Kelley T. Bloomberg News. April 16, 2009). GSK will hold an 85% share of the joint venture; Pfizer will hold 15%. According to a filing with the US Securities and Exchange Commission, GSK Senior Vice President Dominique Limet, a physician, is CEO-designate of the new company.

The lifetime cumulative risk of at least 1 abnormal ocular lesion for an HIV-positive person ranges from 52% to 100%. Ophthalmic involvement can occur during the early phase of HIV infection, and ocular lesions are mainly noted in the posterior segment.1,2

Persons with HIV infection frequently present with anemia from different causes, including use of antiretroviral therapy (typically zidovudine), iron deficiency, vitamin B₁₂ deficiency, opportunistic infections (such as mycobacterial and fungal infections), chronic disease, AIDS-associated malignancies, autoimmune hemolysis, and direct effects of HIV infection itself. A frequently overlooked cause of chronic anemia in HIV-infected persons is parvovirus B19 coinfection.^1-3 We present an illustrative case of unsuspected treatable parvovirus B19 infection in an HIV-positive person with chronic transfusion-dependent anemia initially attributed solely to zidovudine therapy.

With the FDA approval of a new small-molecule drug to treat HIV infection by blocking the CCR5 chemokine receptor and with several other drugs of this class in development for this and other indications, there is an increased interest in determining the potential influence on tumor promotion or suppression that blocking this receptor may have. Large, long-term clinical studies would be the ideal method for evaluating the potential increase in cancer risk, and at least one such study is under way (see http://clinicaltrials.gov/show/NCT00665561?order=49).

A 30-year-old white man with HIV infection since September 2004 presented to his infectious disease physician in January 2007 to restart his antiretroviral therapy. Three months earlier, he had discontinued all of his antiretroviral medications because of his loss of health insurance. He remained asymptomatic during this period, with the exception of some mild oral candidiasis.

In a previous Editorial here, I discussed the need for broader uptake of the 2006 CDC recommendations for routine voluntary HIV screening.1

It was the best of times, it was the worst of times. At least that’s how I recall how Charles Dickens begins his story of the civil and personal turmoil during the French Revolution. The United States is in the midst of our own tale of two cities,

Herpes zoster, or shingles, is characterized by unilateral radicular pain and a vesicular rash that is generally limited to a single dermatome. It results from reactivation of latent varicella-zoster virus (VZV) within the sensory ganglia.

The patient is a 54-year-old man, a native of Poland who has lived in the United States for many years. A diagnosis of AIDS was made in 1994, when Hodgkin disease (nodular sclerosing Hodgkin lymphoma) was found in an enlarged cervical lymph node and he tested positive for HIV during his workup.

In a recent AIDS Reader editorial, Joel E. Gallant called for clinicians who treat persons with HIV/AIDS to “become vocal advocates for routine HIV screening,”1 in line with recent CDC recommendations to screen all patients between the ages of 13 and 64 in US health care settings.2 One of the citations in that editorial was particularly telling: “Why don’t physicians test for HIV?”3

Prolonged exposure to high-risk strains of human papillomavirus (HPV) and the dysplastic effects that HPV exerts on cells of the squamocolumnar transitional junction of the anal canal lead to anal intraepithelial neoplasia (AIN), which is a precursor to squamous cell carcinoma of the anus (SCCA).1