Clinical characteristics of the novel coronavirus infection in HIV-positive patient with underlying chronic hepatitis C
* Impact factor according to the SCIENCE INDEX 2021
I.A. Matyazh1, E.V. Ivakhnenko1, A.V. Grokhotova2
1City Infectious Diseases Hospital, Sevastopol, Russian Federation
2Institute "S.I. Georgievsky Medical Academy", V.I. Vernadsky Crimean Federal University, Simferopol, Russian Federation
In view of the global pandemic caused by the novel coronavirus disease, HIV-infected people fall into a higher risk group, as they have a weakened immune system and underlying health conditions. Currently, much research focuses on the clinical characteristics of the coronavirus infection in various population groups with comorbidities, including HIV-positive patients. The article describes the clinical course of the novel coronavirus diseases in a male patient, 44 years of age, newly diagnosed with HIV at the time of hospitalization, who also had chronic hepatitis C with low specific enzyme levels. The chest CT scans demonstrated multiple polygonal sites of increased attenuation of the lung parenchyma (ground glass opacities) in segments S2, S3, S4, S5, S6–S10 of the right lung and in S3, S6–S10 segments of the left lung; these changes were more pronounced in the right lung. Most of the sites were detected in the subpleural region and close to the lung roots. Th e absence of highly active antiretroviral therapy resulted in a severe immunosuppression — during patient’s stay at the hospital the number of leucocytes decreased from 3.62×109/l to 2.54×109/l. However, in the entire period of illness, his condition remained stable (moderate severity), and no complications were reported.
Keywords: HIV-infection, chronic hepatitis C, COVID-19, novel coronavirus infection.
For citation: Matyazh I.A., Ivakhnenko E.V., Grokhotova A.V. Clinical characteristics of the novel coronavirus infection in HIV-positive patient with underlying chronic hepatitis C. Russian Medical Inquiry. 2022;6(11):656–658 (in Russ.). DOI: 10.32364/2587-6821-2022-6-11-656-658.
Given the ongoing COVID-19 pandemic, individuals infected with HIV who are characterized by a weakened immune system compared to the general population and the presence of chronic comorbidities are at high risk for the disease [1, 2].
Extensive studies on the epidemiology and clinical signatures of the COVID-19 in different groups with various comorbidities (including HIV-positive patients) are underway, and novel treatment and preventive approaches are being developed [3, 4]. The most common respiratory illness manifests as bilateral pneumonia, and acute respiratory distress syndrome occurs in 15–30% [5, 6]. Hypercoagulation with thromboembolism is less common. Disorders of other systems and organs, i.e., central nervous system, gastrointestinal tract, immune system, endocrine system, myocardium, liver, and kidneys, are also reported. In severe COVID-19, sepsis and septic shock develop .
From January 1, 2020, to June 30, 2020, coinfection with HIV and SARS-CoV-2 was detected in 1 of 235 patients with the COVID-19 registered in Sevastopol (0.42%). We describe this case report.
A 44-year-old man was admitted to the hospital on March 11, 2020, for bilateral viral pneumonia. During the in-hospital stay, he has been in contact with a COVID-19 patient, and therefore, he was transferred to another hospital for observation. At admission, chest X-ray revealed an opacity with blurred margins in the right lung and an abnormal pulmonary pattern of the root of the right lung. Meanwhile, pulmonary sinuses were clear, the normal appearance of heart and aortic shadows was reported. Right-sided pneumonia was diagnosed. On April 18, 2020, computed tomography (CT) of the chest was performed. Chest CT revealed signs of bilateral pneumonia (multiple polygonal ground-glass opacities in S2, S3, S4, S5, and S6–S10 of the right lung and S3 and S6–S10 of the left lung, R>L). These opacities were mainly located in the subpleural space and root areas. Moreover, an area of severe angular deformity of the pulmonary pattern amid pulmonary consolidation was detected in S6–S10 of the right lung. The total size of the consolidation in S10 of the right lung was 41×31×30 mm. The rest of the lung fields (upper lobes) were regularly pneumatized. By day 5 of in-hospital stay, the patient complained of headache, cough, shortness of breath, subfebrile temperature.
On April 20, 2020, the patient was transferred into infectious disease hospital with suspected COVID-19. The preliminary diagnosis was bilateral viral pneumonia and suspected COVID-19 (ICD-10-CM codes Z03.8 and J18.9). SARS-CoV-2 RNA was found in nasopharyngeal and oropharyngeal swabs using the Vector-PCRv2019-nCoV-RG test system. The patient was diagnosed with the laboratory-confirmed moderate-to-severe COVID-19, moderate community-acquired pneumonia, and respiratory insufficiency grade 1 (ICD-10-CM codes U07.1 and J12.8) based on medical history, examination, and laboratory and instrumental tests.
On admission to infectious disease hospital (April 20, 2020), the condition was fair, the patient was conscious, no meningeal signs were reported. The skin was pale (no cyanosis), normal appearance of mucous membranes, no throat redness, and no tonsillar swelling or patches were reported. Chest auscultation revealed left-sided diminished breath sounds and fine crackles in the middle sections. Heart sounds were somewhat muffled, rhythmic, no murmurs. The abdomen was soft, slightly painful in the right hypochondrium, the liver was 2 cm below the costal margin, the spleen was not palpable. No peripheral edema was detected. Urination was regular and painless. The poop was well-formed, no abnormalities.
During the in-hospital stay, the patient was first tested positive for HIV with manifestations of multiple infections (stage 4, progression of HIV to AIDS, no highly active antiretroviral therapy/HAART) and weight loss of 17% (with respect to reference values). Additionally, hepatitis C with low liver enzyme levels was diagnosed. A cellular immunity test (April 24, 2020) revealed severe immunosuppression, i.e., absolute lymphocyte count was 0.87 × 109/l, CD4 count was 69.6 cells/μl (8%), CD8 count was 74%, and CD4/CD8 ratio was 0.1.
The patient received cotrimoxazole 480 mg QID for 30 days, umifenovir 200 mg QID for 14 days, interferon α2b (double dose) 5 times a day for 14 days, fluconazole 50 mg daily for 30 days, IM ceftriaxone 2 g daily for 10 days, glycyrrhetinic acid phospholipid complex 1 drop TID for 11 days, cefepime 1 g BID for 10 days, and acyclovir 400 mg TID. During the in-hospital stay, the patient underwent regular chest CT to monitor treatment efficacy. As mentioned above, bilateral viral pneumonia and an area of severe angular deformity of the pulmonary pattern in S6–S10 of the right lung sized 41×31×30 mm was identified on April 18, 2020. Follow-up scans (May 2 and May 14, 2020) demonstrated an improvement, i.e., a reduction in the number and size of opacities, fibrosis began to develop in S9–S10 of the right lung.
Changes in CBC (April 21 and May 19, 2020) during treatment were positive and demonstrated viral origin of the disease. Meanwhile, a reduction in WBC counts illustrated the enhancement of immunosuppression during the COVID-19 in this HIV-positive patient who required treatment. Thus, hemoglobin level increased from 122 g/l (at admission) to 130 g/l, WBC count decreased from 3.62×109/l to 2.54×109/l, ESR reduced from 35 mm/h (at admission) to 9 mm/h, neutrophil levels reduced from 60.5% to 36.6%, platelet count reduced from 154 × 109/l to 145 × 109/l. The levels of lymphocytes, monocytes, eosinophils and basophils slightly increased (from 24% to 42%, from 11.1% to 18.9%, from 1.9% to 2%, and from 0.3% to 0.4%, respectively). Blood biochemistry parameters (April 21 and May 19, 2020) were within normal limits, excepting ALT (that decreased from 54.6 to 34.2 U/l) and AST (that increased from 55.4 to 60.1 U/l). Urinalysis parameters were within normal limits.
The duration of treatment in the infectious disease hospital was 30 days (from April 20 to May 19, 2020). COVID-19 course in this HIV-positive patient was favorable with further recovery. Despite severe immunosuppression (less than 100 cells/µl) and the lack of HAART, by day 27 of the disease, body temperature was normal, no shortness of breath was reported, cough was scarce and appeared mainly in the morning. The condition improved, but moderate weakness and fatigue persisted. Organ and system functioning was stable. The patient was discharged to be followed up by a therapist. He was also referred to the phthisiatrician for prescribing tuberculosis chemoprophylaxis to further introduce it into HAART. Finally, cotrimoxazole 480 mg TID to an increase in CD4 count >200 cells/μl, acyclovir 400 mg TID, and fluconazole 50 mg BID to an increase in CD4 count >100 cells/μl were recommended to prevent opportunistic infection.
As COVID-19 incidence increases, the disease is assumed to be more severe in HIV-positive patients due to impaired immunity . A higher infection rate, morbidity, and mortality were expected in this population . However, the analysis of COVID-19 incidence in HIV-positive patients over 6 months demonstrates a relatively low infection with SARS-CoV-2 and mild uncomplicated course of the COVID-19. The lack of laboratory-confirmed cases of COVID-19 in HIV-positive patients (excepting this case report) in Sevastopol suggests that these patients have a much lower risk of being infected with SARS-CoV-2 due to HAART and predominantly mild course of the disease. These patients remain epidemiologically undetected because of the lack of most symptoms of the COVID-19. Unfortunately, we failed to establish reliably the time of HIV infection, and therefore, to analyze the effect of disease duration on COVID-19 course.
This case report describing a patient with impaired immunity (because of two diseases, HIV/AIDS and hepatitis C) and uncomplicated COVID-19 of moderate severity is in contrast with the idea of a more severe course of COVID-19 in immunocompromised patients. This phenomenon requires further studies to elucidate the specifics of COVID-19 in HIV-positive patients.
About the authors:
Inga A. Matyazh — Chief Physician, City Infectious Diseases Hospital of Sevastopol; 40, Kommunisticheskaya str., Sevastopol, 299003, Russian Federation.
Elena V. Ivakhnenko — Infectious disease specialist of the Outpatient Polyclinic Department "Center for HIV Prevention," City Infectious Diseases Hospital; 40, Kommunisticheskaya str., Sevastopol, 299003, Russian Federation; ORCID iD 0000-0002-2336-3512.
Anastasia V. Grokhotova — Postgraduate student of the Institute "S.I. Georgievsky Medical Academy", V.I. Vernadsky Crimean Federal University; 5/7, Lenin blvd., Simferopol, 295007, Russian Federation; ORCID iD 0000-0003-0740-0763.
Contact information: Anastasia V. Grokhotova, e-mail: firstname.lastname@example.org.
Financial Disclosure: no authors have a financial or property interest in any material or method mentioned.
There is no conflict of interests.
2. Zhu F., Cao Y., Xu S., Zhou M. Co-infection of SARS-CoV-2 and HIV in a patient in Wuhan city, China. J Med Virol. 2020;92(6):529–530. DOI: 10.1002/jmv.25732.
3. Coleman H., Snell L.B., Simons R. et al. Coronavirus disease 2019 and Pneumocystis jirovecii pneumonia: a diagnostic dilemma in HIV. AIDS. 2020;34(8):1258–1260. DOI: 10.1097/QAD.0000000000002571.
4. Larzábal F.J., Vilela A., Brusca S. et al. [Simultaneous diagnosis and favorable evolution of infection with Pneumocystis jirovecii, SARS-CoV-2 and advanced HIV]. Medicina (B Aires). 2020;80(5):554–556.
5. Yano H., Nakano R., Suzuki Y. et al. Inactivation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by gaseous ozone treatment. J Hosp Infect. 2020;106(4):837–838. DOI: 10.1016/j.jhin.2020.10.004.
6. Attaway A.H., Scheraga R.G., Bhimraj A. et al. Severe COVID-19 pneumonia: pathogenesis and clinical management. BMJ. 2021;372:n436. DOI: 10.1136/bmj.n436.
7. Choudhary S., Sharma K., Silakari O. The interplay between inflammatory pathways and COVID-19: A critical review on pathogenesis and therapeutic options. Microb Pathog. 2021;150:104673. DOI: 10.1016/j.micpath.2020.104673.
8. Gatechompol S., Avihingsanon A., Putcharoen O. et al. COVID-19 and HIV infection co-pandemics and their impact: a review of the literature. AIDS Res Ther. 2021;18(1):28. DOI: 10.1186/s12981-021-00335-1.
9. Lesko C.R., Bengtson A.M. HIV and COVID-19: Intersecting Epidemics With Many Unknowns. Am J Epidemiol. 2021;190(1):10–16. DOI: 10.1093/aje/kwaa158.
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